Background: Hepatic ischemia reperfusion injury (HIRI) is considered one of the most common causes of liver damage and dysfunction. Oxytocin (OT), besides its classical functions, exhibits a potent antistress, anti-inflammatory, and antioxidant effects. Aim: This study was designed to evaluate the effect of pretreatment with OT on HIRI and to determine its possible protective mechanisms, focusing on the potential role of NADPH oxidase 2 (NOX2). Methods: 28 adult Wister albino male rats were divided into 4 groups: group I (control group): received saline and subjected to surgery without ischemic procedure, group II (OT group): received OT and subjected to surgery without ischemic procedure, group III (HIR group): underwent hepatic ischemia reperfusion (HIR) procedure & group IV (HIR+ OT group): received OT and underwent HIR procedure. We assessed the effect of OT on serum liver enzymes, hepatic malondialdehyde (MDA), glutathione (GSH), tumor necrosis factor alfa (TNFα), and NOX2. Results: HIR caused significant increase in serum liver enzymes, hepatic MDA, TNFα and NOX2 levels with a significant decrease in GSH level. Administration of OT caused a significant improvement in all previous parameters, these results were supported by histopathological examination. Conclusion: OT exerts hepatoprotective effect in HIR-induced liver injury even in part through NOX2.
Senile osteoporosis (SOP) is a degenerative bone disease associated with increasing susceptibility to fractures and mortality in the elderly. Innate immunity and specifically the nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, with its subsequent mediators caspase1and interlukin-1b (IL-1b),have recently been linked to osteoporosis. Probiotic lactobacillus acidophilus (L.A) was reported to exert favorable effects on osteoporosis.The aim of this study was to identify the protective effects of probiotic L.A in aged osteoporotic rat model and to evaluate the possible underlying mechanisms focusing on NLRP3 inflammasome and its effectors caspase-1 and interleukin -1b. Thirty-two adult male albino rats were designated to four equivalent groups. Group I; control, group II; probiotic L.A, group III; osteoporotic group, and group IV; probiotic LA+ osteoporosis group. Osteoporotic rats pretreated with L.A in a dose of 10 9 CFU/ml / day for 8 weeks revealed a significantly lower oxidative stress state, increased bone mineral density (BMD), enhanced bone histological architecture, lower serum calcium, higher bone formation markers associated with lower bone resorption marker, lower serum receptor activator of nuclear factor kappa-Β ligand (RANKL), decreased bone NLRP3 inflammasome as well as caspase-1 expression levels and lower serum IL-1b.Osteoprotective effects of probiotic L.A in SOP rat model mediated even in part via its anti-inflammatory effects that was represented by decreased NLRP3 inflammasome and its subsequent mediators caspase-1 and IL-1b, that resulted in enhancement of bone formation and reduction of bone resorption.
Non-alcoholic fatty liver disease (NAFLD) represents a growing cause of liver morbidity and mortality globally with no proven effective therapy yet. The aim of this research is to investigate the effect of vitamin D treatment on choline deficient (CD) diet-induced nonalcoholic fatty liver disease (NAFLD) like lesions in rats, with the possible involvement of irisin in this effect. Thirtytwo rats were divided into 4 equal groups; control group, vitamin D group, CD diet group, CD diet+ vitamin D group. It was found that CD diet led to significant elevations in liver weight and index, serum liver enzymes, hepatic triglycerides (TG), malondialdehyde (MDA), inflammatory markers with significant decreases in serum 25-(OH) D3, irisin, hepatic antioxidants and peroxisome proliferator-activated receptor alpha (PPAR-α). Administration of vitamin D caused a significant improvement in all previous parameters, these results were supported by histopathological examination. It seems that vitamin D supplementation significantly reduced NAFLD induced by CD diet even in part due to irisin. Keywords-Irisin -vitamin D -fatty liver Bull. of Egyp. Soc. Physiol. Sci.
With recent upsurge in obesity, the prevalence of nonalcoholic fatty liver disease (NAFLD) is growing globally. The objective of this study was to investigate the influence of erythropoietin (EPO) therapy on NAFLD and the role of transforming growth factor beta one (TGFβ1). NAFLD was induced in adult male albino Wistar rats by administration of methionine choline deficient (MCD) diet. Serum level of aspartate aminotransferase (AST), alanine aminotransferase (ALT), albumin, bilirubin, triglycerides (TG), total cholesterol (TC), body weight, liver weight and liver weight /body weight ratio were measured in different experimental groups to assess the liver affection. Liver samples were taken for measurement of TG, TC, malondialdehyde (MDA), reduced glutathione (GSH) and tumor necrosis factor alpha (TNF-α) as well as histopathological detection of hepatic tissue injury and immuno-histochemical assessment of TGFβ1. As compared to the control group, MCD diet was found to produce a significant increase in serum level of AST, ALT, liver weight and liver weight/ body weight ratio, accompanied with a significant increase in liver tissue MDA, TNF-α and TGF-β1 immuno-histochemical scoring. However, there was a significant decrease in hepatic GSH level. It also resulted in significant elevation in hepatic TG and TC, significant decrease in serum TG and TC levels and non-significant change in body weight, serum albumin and bilirubin. These results were supported by histopathological changes in hepatic tissues in the form of steatosis of hepatocytes and inflammatory cells infiltration. These results were reversed by EPO treatment. EPO treatment showed a hepato-protective effects against the development of NAFLD with a significant preservation of liver functions and structure that could be explained by the anti-oxidant, anti-inflammatory and anti-fibrogenic effect of EPO treatment.
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