Autophagy is necessary for neuronal homeostasis and its dysfunction has been implicated in Parkinson's disease (PD) as it can exacerbate endoplasmic reticulum (ER) stress and ER stress-induced apoptosis. Quercetin is a flavonoid known for its neuroprotective and antioxidant effects. The present study investigated the protective, autophagy-modulating effects of quercetin in the rotenone rat model of PD. Rotenone was intraperitoneally injected at dose of 2 ml/kg/day for 4 weeks. Simultaneous intraperitoneal injection of quercetin was given at a dose of 50 mg/kg/day also for 4 weeks. Neurobehavioral changes were studied. Oxidative/antioxidant status, C/EBP homologous protein (CHOP), Beclin-1, and dopamine levels were assessed. DNA fragmentation and histopathological changes were evaluated. This research work revealed that quercetin significantly attenuated rotenone-induced behavioral impairment, augmented autophagy, ameliorated ER stress- induced apoptosis with attenuated oxidative stress. From the current study, quercetin can act as an autophagy enhancer in PD rat model and modulates the microenvironment that leads to neuronal death.

To evaluate the potential role of sphingosine-1-phosphate receptor agonist, fingolimod (FTY-720), in rat I/R induced testicular injury and its possible underlying protective mechanisms. Experimental protocol: Thirty male albino rats were categorized into three groups, 10 rats each: sham operated control group, Ischemia/Reperfusion (I/R) group: underwent torsion/detorsion procedures of the left testes and FTY720 treated (I/R+FTY720) group: received single FTY720 injection (at a dose of 4 mg/kg i.p) 30 min. before detorsion. At the end of the ischemia and reperfusion period (4 h) left testes were dissected carefully in all rats for histological and biochemical investigations. Testicular malondialdehyde (MDA), testicular antioxidant enzymes and testicular sphingolipids were assessed. Results: FTY720 treatment of I/R group resulted in significant reduction in I/R induced elevation in testicular GSH-Px, SOD, MDA and total ceramide level, along with significant increase in testicular catalase, sphingomyelin and sphingosine-1-phosphate. Also, FTY720 treatment of I/R group improved severe testicular injury changes in I/R group. Conclusion: FTY treatment may be used as potential therapeutic treatment for I/R induced testicular injury.

Background: The epidemic of obesity has contributed to the rapid rise in comorbid conditions such as cardiovascular disease, type 2 diabetes mellitus and hypertension. Aim of Study: The aim of this study was to determine the effect of exercise on metabolic disorders and mitochondrial dysfunction associated with obesity. Material and Methods: The study was conducted on 60 male albino rats divided randomly into four equal groups: Group I: Control non-trained group; Group II: Obese nontrained group; Group II: Control trained group and Group IV: Obese trained group. Obesity was induced by hydrating rats with 70% fructose solution for 5 weeks. Following induction of obesity and after 8 consecutive weeks of swimming exercise, citrate synthase enzyme activity was measured by a kinetic spectrophotometric assay. Plasma insulin level was measured by ELISA and insulin resistance was assessed using (HOMA-IR index), while plasma levels of glucose, triglycerides and total cholesterol were determined by colorimetric assay. Results: The levels of glucose, total cholesterol, triglycerides and insulin resistance were significantly increased in obese non-trained group but significantly decreased in obese trained group compared to control groups. Also citrate synthase activity was significantly increased in obese trained group compared to obese non-trained group. Conclusion: Endurance exercise results in improvement of obesity and glucose homeostasis.