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Background: diabetic myopathy is one of chronic complications of diabetes mellitus, which is evidenced by muscle weakness and atrophy. In our research we aimed to evaluate the protective role of exercise and vitamin D on diabetic induced changes in the skeletal muscles. Methods: Forty male Sprague Dawely rats were divided into control, diabetic, exercised diabetic, vitamin D treated diabetic and combined exercise and vitamin D diabetic rats. Fasting blood glucose, fasting insulin, HOMA-IR, serum IGF-1 level as well as the contractile properties of soleus and tibialis anterior muscles were measured. Also western blot analysis for measuring (LC3) and histopathological examination of both muscles were done. Results: in diabetic rats, fasting blood glucose, fasting insulin, HOMA-IR and LC3 (microtubule associated protein-1 light chain-3) expression in muscles were increased whereas serum IGF-1 level was decreased and the contractile properties of skeletal muscles were deteriorated. Vitamin D treatment decreased fasting blood glucose, fasting insulin, HOMA-IR and expression of LC3 but it increased serum IGF-1 with improvement in the skeletal muscles' contractility. Also exercised diabetic rats revealed improvement in all biochemical parameters, autophagy marker expression with further improvement in the skeletal muscles' contractility. Combining exercise and vitamin D treatment showed a more improvement in all studied parameters and the histopathological examination confirmed our results. Conclusion: regular exercise and vitamin D protect the muscles from diabetic induced lesions by improving glycemic state, serum level of IGF-1and suppressing autophagy which finally reflected on the contractile parameters of the muscles.

Aim of the work: the present study aims at testing whether chronic hypoxia alters the dilator vascular responses of rat carotid circulation to adenosine-evoked fall in arterial blood pressure (ABP). The arterial blood pressure was lowered to the lower limit of cerebral autoregulatory range giving the chance to further study whether the carotid autoregulatory response to adenosine-evoked fall in ABP is compromised by chronic hypoxia or not. A third aim is to investigate whether the role of tonically synthesized nitric oxide (NO) in dilator responses evoked by adenosine in carotid vasculature is different in chronic hypoxic rats. Study Design: the study was done using 2 comparable age groups of adult male Wistar rats; the first were breathing normal 21% O 2 (normoxic; N), whereas the second were made chronically hypoxic (CH) by breathing 12% O 2 for 3 weeks, while they were growing from 7 to 10 weeks. In anaesthetized rats, the carotid blood flow (CBF) and carotid vascular conductance (CVC) were recorded during a 3 min infusion of adenosine adjusted at a dose aimed at lowering ABP to 60 mm Hg, the lower limit of autoregulatory range before and after a bolus dose of the nitric oxide synthase inhibitor L-NAME (10mg.kg-1). Results: in chronic hypoxic rats, the adenosine-induced fall in ABP was associated with a significant increase in CVC but with no significant increase in CBF in contrast to the significant increase in CBF noticed in N rats. Also, adenosine-evoked increase in baseline CVC was significantly larger in N than in CH rats. Inhibition of nitric oxide synthase produced comparable changes on baseline values in CH as in N rats. In CH rats, L-NAME did not attenuate the increase in CVC evoked by adenosine as it did in N rats. However, after L-NAME, CBF increased in CH rats. Conclusion: From these results, it could be suggested that exposing rats to chronic hypoxia for 3 weeks does not compromise the carotid autoregulatory response to the fall in arterial blood pressure. However, it seems that adenosine does not exert an active vasodilatation in carotid circulation of CH rats as it does in N rats. Further, it seems that the adenosine-evoked increase in CBF in CH rats is largely nitric oxide-independent.

The aim of this study was to investigate the possible protective role of Hydrogen sulfide (H 2 S) on chronic unpredictable stress (CUS) -induced gastric lesions in rats. Materials and methods: 40 rats were divided into 4 groups: control group, stressed rats group, stressed + Aminooxyacetic acid (AOAA) (inhibitor of H 2 S synthesis; 50mg/kg/48hour; IP), stressed + Sodium hydrosulfide (NaHS) (donor of H 2 S, 5mg/kg/48hour; IP). In all the groups exposed to CUS, a set of chronic unpredictable stressors was applied for 6 weeks in random order. At the end of experimental protocol blood samples, gastric content and gastric tissues samples were collected. Gastric tissues histopathological changes were evaluated by macroscopic and microscopic examination. Gastric content pH, serum MDA level, whole blood GSH level were estimated. Expression of Caspase-3 (apoptotic marker) and BCL-xl (anti-apoptotic marker) was assessed by immunohistochemistry. Results: In all the groups exposed to CUS, there was a significant reduction in gastric pH value and a range of gastric lesions ranging from superficial to deep ulceration as evident by macroscopic and microscopic examination. Also, there was significant elevation in MDA serum level and significant reduction in anti-oxidant GSH blood level. In all stressed rats, the expression of Caspase-3 was significantly higher whereas a significant decrease in expression of anti-apoptotic protein BCL-xl was observed. These findings were aggravated by AOAA while using NaHS improved them. Conclusion: it seems that increasing bioavailability of H 2 S could have a protective role against CUS induced gastric lesions. The results suggest that this protection could be through anti-oxidant and anti-apoptotic effects Keywords• hydrogen sulfide (H2S)• Chronic unpredictable stress (CUS)• Caspase 3Bull. of Egyp. Soc. Physiol. Sci.

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