Int J Physiol Pathophysiol Pharmacol [JOURNAL]
Sun
200 papers
Application of weighted gene co-expression network analysis to identify the hub genes in H1N1.
Sun B, Guo X, Wen X … +5 more , Xie YB, Liu WH, Pang GF, Yang LY, Zhang Q
Int J Physiol Pathophysiol Pharmacol · 2021 · PMID 34336131
OBJECTIVE: Identifying the disease-associated interactions between different genes helps us to find novel therapeutic targets and predictive biomarkers. METHODS: Gene expression data GSE82050 from H1N1 and control human...
OBJECTIVE: Identifying the disease-associated interactions between different genes helps us to find novel therapeutic targets and predictive biomarkers. METHODS: Gene expression data GSE82050 from H1N1 and control human samples were acquired from the NCBI GEO database. Highly co-expressed genes were grouped into modules. Through Person's correlation coefficient calculation between the module and clinical phenotype, notable modules were identified. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were conducted, and the hub genes within the module of interest were identified. Also, gene expression data GSE27131 were acquired from the GEO database to verify differential key gene expression analysis. The CIBERSORT was used to evaluate the immune cells infiltration and the GSVA was performed to identify the differentially regulated pathways in H1N1. The receiver operating characteristic (ROC) curves were used to assess the diagnostic values of the hub genes. RESULT: The black module was shown to have the highest correlation with the clinical phenotype, mainly functioning in the signaling pathways such as the mitochondrial inner membrane, DNA conformation change, DNA repair, and cell cycle phase transition. Through analysis of the black module, we found 5 genes that were highly correlated with the H1N1 phenotype. The H1N1 project from GSE27131 confirmed an increased expression of these genes. CONCLUSION: By using the WGCNA we analyzed and predicted the key genes in H1N1. BRCA1, CDC20, MAD2L1, MCM2, and UBE2C were found to be the most relevant genes, which may be therapeutic targets and predictive biomarkers for H1N1 therapy.
Multi-organ protective effect of on low concentration toxic metal mixture in albino rats.
Anyanwu BO, Orish CN, Ezejiofor AN … +3 more , Nwaogazie IL, Akaranta O, Orisakwe OE
Int J Physiol Pathophysiol Pharmacol · 2021 · PMID 34093966
Heavy metal mixture can induce multiple organ damage through oxidative stress and inflammatory processes. Dietary intervention using natural antidotes in resource poor countries where classical metal chelators are either...
Heavy metal mixture can induce multiple organ damage through oxidative stress and inflammatory processes. Dietary intervention using natural antidotes in resource poor countries where classical metal chelators are either not affordable or available can be explored as an alternative means of management of public health effects of chronic heavy metal exposure. The search for natural antidote against the deleterious effects of heavy metals gives the thrust for this study. Thus, the study investigated the effect of aqueous leaf extract of on liver, kidney, brain and testis induced by low dose heavy metal mixture (LDHMM) of PbCl, CdCl and HgCl of concentrations of 20 mg/kg, 1.61 mg/kg and 0.40 mg/kg, respectively. Five groups of seven rats each (weight-matched) were used. First and second groups received deionized water and heavy metal mixture and served as normal and toxic controls, respectively. Groups 3, 4 and 5 received through oral gavage 750, 1500, 2250 mg/kg of the extract respectively, with the metal mixture concurrently. All treatments were four times a week for 90 days (4/week/90 days). Hepatorenal, hormonal, oxidative stress markers, cytokines (interleukin-6 and interleukin-10), and heavy metals (Pb, Cd and Hg) concentrations were assayed. The one-way analysis of variance, agglomerative hierarchical clustering, parallel coordinates plot, principal component analysis and Bray Curtis dissimilarity were used to statistically analyze the data. LDHMM caused significant changes in these organs and however, the plant extract provided a protective effect against these pathological changes. The statistical analysis revealed that the kidney was the most affected organ, followed by the liver, then brain and testis, respectively. may be an important nutraceutical in multi-organ deleterious effects of LDHMM following its regulation of oxidative stress markers, inflammatory cytokines and biometal chelation.
Zinc cytotoxicity induces mitochondrial morphology changes in hela cell line.
Knies KA, Li YV
Int J Physiol Pathophysiol Pharmacol · 2021 · PMID 34093965
Zinc (Zn) is important in cellular processes. In the cell, free zinc is tightly regulated and found in minuscule amounts. However, in an unhealthy cellular environment, such as hypoxia, zinc increases in the cell and zin...
Zinc (Zn) is important in cellular processes. In the cell, free zinc is tightly regulated and found in minuscule amounts. However, in an unhealthy cellular environment, such as hypoxia, zinc increases in the cell and zinc overload may occur. Studies have shown that zinc overload causes cellular and mitochondrial stress. Mitochondrial stress affects mitochondrial morphology. In normal cells, mitochondrial morphology resembles a long, tubular shape. In unhealthy cells, mitochondrial morphology resembles fragmented, circular shape. To address whether zinc overload contributes directly to the abnormal changes of mitochondrial morphology, we imaged and analyzed mitochondria that were treated with the application of exogenous zinc. In the first part of the study, exogenous zinc was applied to HeLa cells at 1 µM, 10 µM, 50 µM, 100 µM, or 200 µM zinc chloride along with 10 µM pyrithione. Mitochondrial morphology was analyzed with Mito-Morphology micro in ImageJ. Mitochondrial morphology changed from a healthy tubular shape to an unhealthy circular shape and fragmentation. Mitochondrial morphology changes were observed in a dose-dependent fashion. The second part of the study involved applying the metal ion chelator TPEN after applying 50 µM zinc chloride along with 10 µM pyrithione. TPEN reduced zinc-induced abnormal mitochondrial morphology after zinc treatment. This present study supports that zinc overload may cause morphology changes induced by mitochondrial stress that may lead to cell death.
A cross-sectional cadaveric study of the correlation between genital organ measurements, serum testosterone, and serum prostate-specific antigen levels in Japanese male subjects.
Takeshima Y, Suzuki M, Ikegaya H … +4 more , Idota N, Kawai T, Sato Y, Kume H
Int J Physiol Pathophysiol Pharmacol · 2021 · PMID 34093964
Association of organ sizes in the genitalia have long been a topic of interest for the general public. However, factors such as selection bias, embarrassment, and invasive testing have hindered studies on living individu...
Association of organ sizes in the genitalia have long been a topic of interest for the general public. However, factors such as selection bias, embarrassment, and invasive testing have hindered studies on living individuals. We obtained measurements of penile size, testicular weight, and prostate weight, and conducted related serum testing on 63 Japanese male adults who died of unexpected reasons and underwent autopsy from 2009 to 2013. Micropenis was seen in 7 subjects (11.1%) as determined by flaccid penile length. Penile measurements were mainly correlated with body weight, testicular weight with age and body mass index, and prostate weight with age and serum prostate-specific antigen level. No correlation was detected between testosterone and any genital organ measurements. Interestingly, penile circumference showed no correlation to any of the penile length measurements. Prostate weight showed a significant positive correlation with penile circumference, penile stretched length, and testicular weight. Although the direct clinical implications are unclear, utilizing autopsy provided insight into genital organ measurements free of patient selection bias and other disadvantages of live patient testing. With a larger sample size, autopsy studies may be of use to future adjustment of nomograms.
The protective effect of olanzapine on ketamine induced cognitive deficit and increased NR1 expression in rat model of schizophrenia.
Mahmoud GS, Hosny G, Sayed SA
Int J Physiol Pathophysiol Pharmacol · 2021 · PMID 34093963
BACKGROUND: Impaired cognitive flexibility is the core manifestation of schizophrenia (SZ). Previous literature raised a claim against the effect of atypical antipsychotic drugs (AAD) on cognitive and executive functions...
BACKGROUND: Impaired cognitive flexibility is the core manifestation of schizophrenia (SZ). Previous literature raised a claim against the effect of atypical antipsychotic drugs (AAD) on cognitive and executive functions whose cause needs further investigation. Attention set-shifting task (ASST) tests the prefrontal cortex's (PFC) executive and flexibility functions. GOALS: To examine Olanzapine (OLZ) effect on ASST, expression of N-methyl-D-aspartate receptor 1 (NMDR-NR1) in prefrontal cortex (PFC), and metabolic comorbidity in ketamine (KET) model of SZ. METHODS: Sixty-two male rats were divided into three groups: 8 for ASST and 30 for open field, ELISA and immunohistochemistry sub-chronic study, and 24 for regular serological and histopathological examination. Rats treated with V: vehicle; K: KET and KO: OLZ plus KET. RESULTS: KET caused significant increase in time, trials, and errors to reach criterion. OLZ co-administration reversed effects of KET in ASST with no reduction of locomotor activity. OLZ normalized KET-induced rise of NR1 expression and protected against KET-induced degenerative changes in hippocampus and PFC. Significant increase in serum liver enzymes, total bilirubin, and lipids with chronic compared to sub-chronic OLZ administration. In contrast, insignificant difference between sub-chronic OLZ and vehicle was found. CONCLUSIONS: Current study demonstrated the efficacy of OLZ to reverse KET-induced cognitive deficits in ASST with neither reduction in NR1 expression in PFC nor metabolic malfunction in the sub-chronic study. It also showed the protective effect of OLZ on KET induced neuronal degeneration and necrosis. We suggest that chronic OLZ treatment-induced-metabolic malfunction might be the cause of time-dependent cognitive deterioration.
Organoid biobanks as a new tool for pre-clinical validation of candidate drug efficacy and safety.
Botti G, Di Bonito M, Cantile M
Int J Physiol Pathophysiol Pharmacol · 2021 · PMID 33815668
The growing need for personalized medicine for cancer patients has enhanced and optimized the production of living tumor organoids that have become optimal preclinical models for the discovery and screening of anticancer...
The growing need for personalized medicine for cancer patients has enhanced and optimized the production of living tumor organoids that have become optimal preclinical models for the discovery and screening of anticancer drugs. The systematic collection and storage of tumor organoids through the establishment of dedicated biobanks will represent a fundamental tool for cancer research and clinical trials.
Keratin 1 plays significant roles in maintaining the survival and oxidative stress state of B16-F10 melanoma cell lines.
Li Y, Zhang M, Ying W
Int J Physiol Pathophysiol Pharmacol · 2021 · PMID 33815667
Keratins play multiple significant biological roles in epithelium. Keratin 1 (K1)/keratin 10 (K10) heterodimer is a hallmark for keratinocyte differentiation. While keratins are absent in normal melanocyte, keratins have...
Keratins play multiple significant biological roles in epithelium. Keratin 1 (K1)/keratin 10 (K10) heterodimer is a hallmark for keratinocyte differentiation. While keratins are absent in normal melanocyte, keratins have been found in both melanoma cell lines and human melanoma. The biological significance of the keratins in melanoma cells has remained unclear. In our current study we applied K1 siRNA to investigate the biological significance of K1 in B16-F10 melanoma cells. We found that as low as a 16% decrease in the K1 level led to significant increases in both apoptosis and necrosis of the cells. Moreover, the mild K1 decrease led to significant increases in both dichlorofluorescein (DCF) and ethidium signals - two indicators of oxidative stress - in the cells. Collectively, our findings have provided the first evidence indicating both a critical role of the K1 in maintaining the survival of melanoma cells and an important role of the K1 in modulating the oxidative stress state of the cells. These findings have exposed new functions of keratins in cancer cells, suggesting that K1 may become a novel therapeutic target for melanoma.
Anti-NMDA receptor encephalitis: a review of mechanistic studies.
Huang YQ, Xiong H
Int J Physiol Pathophysiol Pharmacol · 2021 · PMID 33815666
NMDA receptors (NMDARs) are ion channels gated by glutamate, the major excitatory neurotransmitter in the central nervous system. Anti-NMDA receptor (anti-NMDAR) encephalitis is an autoimmune disease characterized by the...
NMDA receptors (NMDARs) are ion channels gated by glutamate, the major excitatory neurotransmitter in the central nervous system. Anti-NMDA receptor (anti-NMDAR) encephalitis is an autoimmune disease characterized by the presence of autoantibodies against the NMDAR GluN1 subunit. Here we briefly review current advances in the understanding of the mechanisms underlying the pathogenesis of anti-NMDAR encephalitis. The autoantibodies bind to and cross-link the endogenous NMDARs, disrupt the interaction of NMDARs with receptor tyrosine kinase EphB2 leading to internalization and reduced function of NMDARs. Hypofunction of the NMDARs results in impairment in long-term potentiation and deficit in learning and memory, leads to development of depression-like behavior, and lowers the threshold for seizures. Recent development of active immunization models of anti-NMDAR encephalitis provides insight into the inflammation process and paves the way for further studies that may lead to better treatment.
A survey on prognosis of anterior cruciate ligament (ACL) reconstruction surgeries following fixed loop and adjustable loop methods.
Yavari P, Mohammadsharifi G, Fadaei B … +2 more , Talebi S, Akbari M
Int J Physiol Pathophysiol Pharmacol · 2020 · PMID 33500748
BACKGROUND: Anterior cruciate ligament (ACL) rupture is an important disease in the younger population and especially professional athletes followed by trauma. There are different surgical methods for repairing ACL ruptu...
BACKGROUND: Anterior cruciate ligament (ACL) rupture is an important disease in the younger population and especially professional athletes followed by trauma. There are different surgical methods for repairing ACL rupture each having their own prognosis rates. Here in this study, we investigated and compared results of ACL reconstruction after the fixed loop and adjustable loop surgical procedure in patients with ACL rupture. METHODS: In this study, we evaluated 60 patients with ACL rupture and divided them into two groups each containing 30 patients. Fixed loop and adjustable loop ACL repair were performed for each group. Data regarding knee society score, static laxity, and joint range of motion (ROM), patient's satisfaction and returning to normal daily activities were collected and compared between two groups after 6 months follow up using SPSS software. RESULTS: We showed that there was no significant difference between two groups of patients regarding investigated factors (P>0.05). No surgical site infections were also observed during the study. CONCLUSION: Both fixed loop and adjustable loop grafting procedures for ACL repair indicate beneficial results and are effective in patients with ACL rupture. We suggest that orthopedic surgeons could use each of these methods according to their own experience and the patient's condition. There are no significant differences between these two methods in the prognosis of patients.
Circadian dysynchrony among nurses performing shift work at a tertiary care teaching hospital: a preliminary study.
Kant R, Yadav P, Kishore S … +2 more , Kumar R, Bairwa M
Int J Physiol Pathophysiol Pharmacol · 2020 · PMID 33500747
BACKGROUND: Circadian rhythm is intracellular molecular mechanisms, influenced by environmental factors such as light, noise, mealtime, and sleep pattern. Shift work affects the sleep pattern, mealtime and psychological...
BACKGROUND: Circadian rhythm is intracellular molecular mechanisms, influenced by environmental factors such as light, noise, mealtime, and sleep pattern. Shift work affects the sleep pattern, mealtime and psychological aspects of workers. This study aims to compare the effect of shift work on circadian dysynchrony among nurses in two different groups based on the duration of shift work. MATERIAL AND METHOD: It was a cross-sectional, preliminary study done at a tertiary care teaching hospital in North India. The study enrolled 170 nurses (aged <35 years) performing shift duties for last 3 years (group-1) and 1 year (group-2) respectively in a 1:1 ratio. Tools used to collect data were case reporting form (demographic and clinical variables, anthropometric measures), Hamilton Anxiety Rating Scale, and Pittsburg Sleep Quality Index. RESULTS: Mean age of participants was 27.39±2.89 vs. 26.14±2.45 in group 1 and 2. We found significant positive correlation of duration of shift work with diastolic blood pressure (DBP) (P=0.000), systolic blood pressure (SBP) (P=0.001), body fat % (P=0.019), weight (P=0.034), hip circumference (HC) (P=0.000) and also significant difference between means of DBP (P=0.001) and HC (P=0.003) in both groups. Whereas bad sleep quality was found in 79% and 66% of participants in group 1 and 2 respectively, the prevalence of moderate to severe anxiety in groups 1 and 2 was 60% and 37% respectively. CONCLUSION: Long duration of shift work increases the risk of developing cardiometabolic risk factors as a consequence of circadian dysynchrony and varies with the duration of shift work.
Connexin36 localization along axon initial segments in the mammalian CNS.
Thomas D, Senecal JM, Lynn BD … +2 more , Traub RD, Nagy JI
Int J Physiol Pathophysiol Pharmacol · 2020 · PMID 33500746
Electrical synapses formed by gap junctions occur at a variety of neuronal subcellular sites in the mammalian central nervous system (CNS), including at somatic, dendritic and axon terminal compartments. Numerous electro...
Electrical synapses formed by gap junctions occur at a variety of neuronal subcellular sites in the mammalian central nervous system (CNS), including at somatic, dendritic and axon terminal compartments. Numerous electrophysiological studies using mice and rats, as well as computer modelling approaches, have predicted the additional occurrence of electrical synapses between axons near their emergence from neuronal somata. Here, we used immunofluorescence methods to search for localization of the neuronal gap junction-forming protein connexin36 (Cx36) along axon initial segments (AISs) labelled for the AIS marker ankyrinG. Immunofluorescent Cx36-puncta were found to be associated with AISs in several CNS regions of mice, including the spinal cord, inferior olive and cerebral cortex. Localization of Cx36-puncta at AISs was confirmed by confocal single scan and 3D imaging, immunofluorescence intensity profiling and high resolution structured illumination microscopy (SIM). AISs measuring up to 30 µm in length displayed typically a single Cx36-punctum and the incidence of these long AISs displaying Cx36-puncta ranged from 3% to 7% in the inferior olive and in various layers of the cerebral cortex. In the inferior olive, the gap junction associated protein zonula occludens-1 (ZO-1) was found to be co-localized with Cx36-puncta on AISs, indicating that these puncta have some of the molecular constituents of gap junctions. Our results add to the neuronal subcellular locations at which Cx36 is deployed, and raise possibilities for its involvement in novel functions in the AIS compartment.
Effect of high salt intake on plasma lipid profile in pregnant wistar rats.
Ajao FO, Iyedupe MO
Int J Physiol Pathophysiol Pharmacol · 2020 · PMID 33500745
Many physiological and behavioral changes take place during pregnancy to ensure the growth and development of a healthy fetus. This study investigates the effects of high maternal salt intake during pregnancy on lipid pa...
Many physiological and behavioral changes take place during pregnancy to ensure the growth and development of a healthy fetus. This study investigates the effects of high maternal salt intake during pregnancy on lipid parameters in Wistar rats. Twenty female Wistar albino rats (200-250 g) were used for the study. The rats were time-mated and day 1 of pregnancy was determined by the presence of spermatozoa after a vaginal lavage. Animals were then randomly divided into two groups: a standard control diet and high-salt diet (8% NaCl) of 10 rats each. On the 19 day, the animals were fasted overnight and sacrificed under anaesthesia. Blood samples were collected via cardiac puncture for determination of lipid parameters triglyceride (TG), total cholesterol (TC), high density lipoprotein-cholesterol (HDL-c), low density lipoprotein-cholesterol (LDL-c), and very low density lipoprotein-cholesterol (VLDL-c) using enzymatic colorimetric method. Atherogenic indices, triglyceride/HDL-C (TG/HDL-C) and total cholesterol/HDL-C (TC/HDL-C) ratios were calculated. SPSS 21.0 package was used for data analysis and level of significance was analyzed using student t-test. Significance was set at P<0.05. Result showed significant (P<0.05) increases in plasma level of TG, TC, LDL-C VLDL-C, TG/HDL-C and TC/HDL-C ratios in high salt fed pregnant rats compared to control. No significant (P>0.05) change was observed in HDL-C level in high salt fed pregnant rats when compared with control. High salt intake during pregnancy has detrimental effect on maternal lipid profile which can threaten both maternal and the fetal life.
Protective potential of curcumin in L-NAME-induced hypertensive rat model: AT1R, mitochondrial DNA synergy.
Greish SM, Abdel-Hady Z, Mohammed SS … +4 more , Abdel-Hamed AR, Masoud RE, Eltamany DA, Abogresha NM
Int J Physiol Pathophysiol Pharmacol · 2020 · PMID 33224436
BACKGROUND & OBJECTIVES: Hypertension can be induced by inhibiting nitric oxide synthesis with L-NAME, which also has a role in oxidative stress. Curcumin has strong antioxidant property. Our aim was to examine the possi...
BACKGROUND & OBJECTIVES: Hypertension can be induced by inhibiting nitric oxide synthesis with L-NAME, which also has a role in oxidative stress. Curcumin has strong antioxidant property. Our aim was to examine the possible preventive role of curcumin on renal dysfunction secondary to hypertension. MATERIAL & METHODS: Twenty-four adult male Albino rats were divided in four groups: normal (N); curcumin (C; received curcumin 100 mg/kg/day by oral gavage for 10 weeks); hypertensive (H; received L-NAME 40 mg/kg/day in their drinking water for 4 weeks); and hypertensive-curcumin (HC; received L-NAME and curcumin). Arterial blood pressure was evaluated non-invasively for 4 weeks. Rats were then sacrificed for assessment of oxidative stress (catalase, lipid peroxidase, reduced glutathione and superoxide dismutase), renal function and structure, and biomarkers of apoptosis (Bcl-2 and caspase-3). AT1R expression and renal mtDNA integrity were also assessed. RESULTS: Curcumin attenuated the effects of L-NAME on blood pressure and renal function. The renal histopathological changes observed in the L-NAME group were improved by curcumin administration. The expression of Bcl2 and caspase-3 was improved associated with downregulation of AT1R in curcumin treated groups. The antioxidant markers and mtDNA fragmentation show marked increase in hypertensive group which significantly decreased after curcumin treatment. CONCLUSION: Curcumin improved blood pressure elevation renal dysfunction. These improvements mediated through anti-oxidant capabilities and downregulation of AT1R favoring reduced apoptosis and preserved mitochondrial DNA.
Maintenance treatment of transcranial magnetic stimulation (TMS) for treatment-resistant depression patients responding to acute TMS treatment.
Chang J, Chu Y, Ren Y … +3 more , Li C, Wang Y, Chu XP
Int J Physiol Pathophysiol Pharmacol · 2020 · PMID 33224435
A growing body of studies has demonstrated that acute transcranial magnetic stimulation (TMS) therapy for treatment-resistant major depressive disorder (MDD) has achieved significant antidepressant effects and can allevi...
A growing body of studies has demonstrated that acute transcranial magnetic stimulation (TMS) therapy for treatment-resistant major depressive disorder (MDD) has achieved significant antidepressant effects and can alleviate other related symptoms. However, MDD has a high relapse rate, and patients with depressive symptoms can relapse weeks or months after acute TMS treatment. The lack of necessary TMS maintenance protocols after completing acute TMS treatment with full remission might be one of the reasons for the high relapse rates in MDD patients. Thus, investigating post-TMS treatment maintenance guidelines is important for decreasing relapse in treatment-resistant depression patients who had initially responded to acute TMS therapy. Therefore, we recommend a scientific approach to decrease relapse in treatment-resistant depression patients who had initially responded to acute TMS treatment.
Altered gestational outcomes and delayed pubertal onset in prenatally and early postnatally food restricted male and female rats: mitigation by quercetin and kaempferol.
Anachuna KK, Ekhoye EI, Iyare C … +5 more , Katchy N, Ben-Azu B, Adeniyi DB, Daubry TME, Iyare E
Int J Physiol Pathophysiol Pharmacol · 2020 · PMID 32934767
Nutrigenomic malnutrition during pregnancy and early postnatal life has serious consequences on original organ-programing, growth pattern, puberty and quality of life. The aim of this was to investigate the effect of two...
Nutrigenomic malnutrition during pregnancy and early postnatal life has serious consequences on original organ-programing, growth pattern, puberty and quality of life. The aim of this was to investigate the effect of two notable flavonoids, quercetin and kaempferol, with nutrigenomic potentials on prenatal and early postnatal food restrictions or both on gestational outcomes and the onset of puberty in male and females Wister rats. In three sets of experiments consisting of prenatal, postnatal food deprivations or both, rats were distributed into various treatment groups (n = 6). Prenatal food restriction (PrNFR) was initiated by 50% of available diet in pregnancy (days 1-22) simultaneously with quercetin (50, 100 and 200 mg/kg, p.o./day) or kaempferol (50, 100 and 200 mg/kg, p.o./day) until delivery. However, postnatal food restriction (PsNFR) was simulated by litter-increment to 16 pups per mother from postnatal day 2 together with quercetin (50-200 mg/kg, p.o.) or kaempferol (50-200 mg/kg, p.o.) treatments until weaning (day 24) respectively. The last experiment encompasses both protocols with similar treatment protocols. Kaempferol attenuated PrNFR-induced alterations in gestational length compared to PrNFR-control. Quercetin and kaempferol significantly ( < 0.05) normalized nose-length of pups of rats exposed to PrNFR. Quercetin and kaempferol reduced the number of stillbirths due to PrNFR. Both also reduced the delay in pubertal onset as evidenced by normal onset of balanopreputial-separation and vaginal-opening in the PrNFR, PsNFR and PrNFR-PsNFR male and female rats respectively. Together, quercetin and kaempferol prevents prenatal and postnatal malnutrition-induced altered gestational outcomes and pubertal delays in rats.
extract protects against cadmium-induced ovarian toxicity in adult Wistar rats.
Oyewopo AO, Olaniyi KS, Olojede SO … +3 more , Lawal SK, Amusa OA, Ajadi IO
Int J Physiol Pathophysiol Pharmacol · 2020 · PMID 32934766
(HS) is native to tropical and subtropical regions, and its enrichment as a source of antioxidants and phytoestrogen has been documented. The present study investigated effects of HS on ovarian toxicity induced by cadmiu...
(HS) is native to tropical and subtropical regions, and its enrichment as a source of antioxidants and phytoestrogen has been documented. The present study investigated effects of HS on ovarian toxicity induced by cadmium. Adult female Wistar rats were grouped into 4 (n=5/group): Group A received HS (100 mg/kg), group B received cadmium sulphate (5 mg/kg), group C received cadmium sulphate and HS, and group D (control) received 1 ml of distilled water. Cadmium sulphate was administered for five days () followed by oral administration of HS for 28 days. Results showed distortion in the cytoarchitecture of the follicular cells in the ovary of cadmium-treated rats while there was mild or no distortion recorded for the ovary of the rats treated with cadmium and HS. There was also a significant reduction in the serum level of Luteinizing and follicle stimulating hormone of the rats treated with cadmium (group B) when compared with control rats. However, these alterations were attenuated when treated with HS. We concluded that HS has an ovarian protective effect in cadmium-treated adult female rats. Hence the present results suggest that HS extract would be a potential therapeutic agent in ovarian dysfunction.
Monoclonal antibody as an emerging therapy for acute ischemic stroke.
Woods D, Jiang Q, Chu XP
Int J Physiol Pathophysiol Pharmacol · 2020 · PMID 32934765
Acute ischemic stroke (AIS) is the 5 leading cause of death and the leading cause of neurological disability in the United States. The oxygen and glucose deprivation associated with AIS not only leads to neuronal cell de...
Acute ischemic stroke (AIS) is the 5 leading cause of death and the leading cause of neurological disability in the United States. The oxygen and glucose deprivation associated with AIS not only leads to neuronal cell death, but also increases the inflammatory response, therefore decreasing the functional outcome of the brain. The only pharmacological intervention approved by the US Federal Food and Drug Administration for treatment of AIS is tissue plasminogen activator (t-PA), however, such treatment can only be given within 4.5 hours of the onset of stroke-like symptoms. This narrow time-range limits its therapeutic application. Administrating t-PA outside of the therapeutic window may induce detrimental rather than beneficial effects to stroke patients. In order to reduce the infarct volume of an AIS while increasing the time period for treatment, new treatments are essential. Emerging monoclonal antibody (mAb) therapies reveal great potential by targeting signaling pathways activated after an AIS. With successful application of mAb in the treatment of cancer, other therapeutic uses for mAb are currently being evaluated. In this review, we will focus on recent advances on AIS therapy by using mAb that targets the signaling cascades and endogenous molecules such as inflammation, growth factors, acid-sensing ion channels, and N-methyl-D-aspartate receptors. Therefore, developing specific mAb to target the signaling pathways of ischemic brain injury will benefit patients being treated for an AIS.
Effects of fingolimod treatments on alanine transaminase and aspartate transaminase levels in patients with multiple sclerosis.
Joni SS, Cheshmavar M, Shoureshi P … +4 more , Zamani Z, Taoosi N, Akbari M, Afzali M
Int J Physiol Pathophysiol Pharmacol · 2020 · PMID 32714497
INTRODUCTION: Multiple Sclerosis (MS) is a chronic neurological disorder with no known cause or cure. Fingolimod (FTY720) is an oral medication recently approved for the treatment of MS as well as other diseases with aut...
INTRODUCTION: Multiple Sclerosis (MS) is a chronic neurological disorder with no known cause or cure. Fingolimod (FTY720) is an oral medication recently approved for the treatment of MS as well as other diseases with autoimmune aspects. However, the drug is not without side effects. The severity and prevalence of these side effects are not completely understood. One of the most common causes for the patient cessation of fingolimod is an increase in liver enzymes, indicating possible inflammation or damage to liver cells. Alanine transaminase (ALT) and aspartate transaminase (AST) are the most common liver enzymes used as indicators of hepatic health. OBJECTIVES: This three-month prospective cohort study selected patients who were diagnosed with relapsing-remitting MS (RRMS) and who were not taking fingolimod oral treatment. ALT and AST levels were determined for these patients at baseline and then after three months of taking FTY720 to determine if these liver enzymes were changed. METHODS: 36 RRMS patients completed this study, which lasted three months. They were started on 0.5 oral FTY720 after approval from a physician and completion of an AST/ALT blood test. Baseline levels were determined and then taken again three months later. Statistical analysis of these values was performed using P<0.05 as a significance threshold. RESULTS: In this sample of patients, only ALT levels were significantly increased after fingolimod treatment in the general cohort (P=0.00). The general cohort showed an insignificant increase in AST levels. In male and female populations separately, AST was not significantly increased. ALT was only significantly increased in men (P=0.00) and insignificantly increased in women. CONCLUSION: This study further confirms our concerns about fingolimod's possible effects on the liver. While these numbers do support the claim that the drug does on average increase ALT in patient populations, it is important to note that most of these patients have no real hepatic side effects. In addition, previous studies have cited a return to normal ALT and AST levels after cessation of fingolimod, suggesting its effects are temporary and not severely damaged in the usual patient.
Sildenafil reverses the hypertrophy of mice right ventricle caused by hypoxia but does not reverse the changes in the myosin heavy chain isoforms.
Aljanabi MA, Alfaqih MA, Al-Khayat AMA … +1 more , Bataineh HN
Int J Physiol Pathophysiol Pharmacol · 2020 · PMID 32714496
In this study, we investigated the effect of hypoxia and concomitant sildenafil treatment on MHC isoforms in hypoxia-induced hypertrophied right ventricles. Right ventricular hypertrophy was induced in mice by exposing t...
In this study, we investigated the effect of hypoxia and concomitant sildenafil treatment on MHC isoforms in hypoxia-induced hypertrophied right ventricles. Right ventricular hypertrophy was induced in mice by exposing them to hypoxic stimulus (11% ambient oxygen) in a normobaric chamber for 20 days. 45 mice were used in this study, distributed randomly into three groups: the first group served as a control (CO), the second group was exposed to hypoxia for 20 days without sildenafil treatment (HY), and the third group was given sildenafil orally at a dose of 30 mg.kg.day plus exposure to hypoxia for 20 days (HS). Relative amounts of MHC isoforms were calculated using two ELISA kits containing antibodies against α and β MHC, and by SDS-PAGE. Compared with the CO group, the HY group showed a significant increase in right ventricle weight/left ventricle plus septum ratio (Fulton's ratio). The HS group showed a significant decrease in Fulton's ratio compared with the HY group, but not with the CO group. Expression of the MHC-β isoform was significantly increased in the HY group compared with the CO group. There was no significant difference in MHC-β between the HY group and the HS group. Plasma atrial natriuretic peptide level was significantly higher in HY group than HS group and did not return to normal after sildenafil treatment. Conclusion: sildenafil reversed the right ventricular hypertrophy induced by hypoxia but did not decrease the expression of MHC-β to normal levels.
No tight junctions in tight junction protein-1 expressing HeLa and fibroblast cells.
Shi Y, Li R, Yang J … +1 more , Li X
Int J Physiol Pathophysiol Pharmacol · 2020 · PMID 32419902
Tight junctions are important structures that form the barrier of cells and tissues, and they play key roles in maintaining homeostasis of our body. The backbone of the tight junction proteins are claudins, which compose...
Tight junctions are important structures that form the barrier of cells and tissues, and they play key roles in maintaining homeostasis of our body. The backbone of the tight junction proteins are claudins, which composed more than twenty members. The tight junction protein 1 (TJP1), also called ZO-1 (Zonula Occludens-1), is one of the tight junction related proteins, and it is widely used in literature to label tight junctions. Here we showed that TJP1 (ZO-1) is highly expressed in cancerous HeLa cells, fibroblast cells, HUVEC as well as MDCK cells, while claudin-1 is highly expressed in HUVEC and MDCK cells, but not expressed in HeLa and fibroblast cells. We aimed to investigate whether tight junction is present in HeLa and fibroblast cells. We used transepithelial/transendothelial electrical resistance (TEER) to measure tight junction dynamics in these cells. The results showed that there is no TEERs in HeLa and fibroblast cells, while there is relatively high TEER in HUVEC and MDCK cells. Importantly, the TEER in MDCK cells is dramatically reduced after knockdown of TJP1 (ZO-1). These results suggest that TJP1 (ZO-1) cannot be used as a marker of tight junctions in a variety of cells, while TJP1 (ZO-1) may play an important role in regulation of tight junctions in MDCK cells.
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