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Abstract
Background and aims: Despite the plentiful researches that have been conducted to clarify the underling pathophysiology of diabetic nephropathy (DN) and renal ischemia-reperfusion injury (I/R), the end stage renal disease (ESRD) caused by both diseases continues to increase worldwide. So, the need still persists to develop new therapeutic designs for these two models of renal injury. Autophagy is a cellular response to injury which is supposed to play fundamental roles in initiation and progression of DN and renal I/R. The aim of the present study is to shed the light on the potential modulatory effects of vitamin D analogue 222-oxacalcitriol (OCT)3 on the autophagic machinery as well as to clarify the possible interplay between autophagy, apoptosis and cell cycle arrest in determining the cell fate. Method: Sixty adult male albino rats were randomly allocated into 3 main groups, each of which was subdivided into 2 subgroups as follow; Control group: which was subdivided into subgroup Ia (non-diabetic) and subgroup Ib (sham-operated), diabetic group: which was subdivided into subgroup IIa (vehicle-treated) and subgroup IIb (22-oxacalcitriol-treated) and lastly renal I/R group which was subdivided into: subgroup IIIa (vehicle-treated) and subgroup IIIb (22-oxacalcitriol-treated). At the end of the experimental protocol, fasting blood glucose levels, serum 25 (OH) D, renal functions, cytokines and gene expression of autophagy, apoptotic and cell cycle arrest parameters were assessed. In addition, the renal architecture was assessed histologically