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Endocr Metab Immune Disord Drug Targets. 2019 Jan 1. doi: 10.2174/1871530319666190102112844. [Epub ahead of print]

Testicular injury attenuated by rapamycin through induction of autophagy and inhibition of endoplasmic reticulum stress in streptozotocin-induced diabetic rats.

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Shanxi Medical University, Taiyuan, Shanxi. China.
Department of Endocrinology, Second Hospital, Shanxi Medical University, Taiyuan, Shanxi. China.



This study investigated whether rapamycin has the protective effect on the testis of diabetic rats by regulating autophagy, endoplasmic reticulum stress, and oxidative stress.


Thirty male Sprague-Dawley rats were randomly divided into three groups: control, diabetic, and diabetic treated with rapamycin, which received gavage of rapamycin ( after induction of diabetes. Diabetic rats were induced by intraperitoneal injection of streptozotocin (STZ, 65mg. Kg-1). All rats were sacrificed at the termination after 8 weeks of rapamycin treatment. The testicular pathological changes were determined by hematoxylin and eosin staining. The protein or mRNA expression of autophagy-related proteins (Beclin1, microtubule-associated protein light chain 3 (LC3), p62), ER stress marked proteins (CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP), caspase-12), oxidative stress-related proteins (p22phox, nuclear factor erythroid2-related factor 2 (Nrf2)) and apoptosis-related proteins (Bax, B cell lymphoma-2 (Bcl-2)) were assayed by western blot or real-time fluorescence quantitative PCR.


There were significant pathological changes in the testes of diabetic rats. The expression of Beclin1, LC3, Nrf2, Bcl-2 were significantly decreased and p62, CHOP, caspase12, p22phox, and Bax were notably increased in the testis of diabetic rats (P <0.05). However, rapamycin treatment for 8 weeks significantly reversed the above changes in the testis of diabetic rats (P <0.05).


Rapamycin appears to produce the protective effect on the testes of diabetic rats by inducing the expression of autophagy and inhibiting the expression of ER-stress, oxidative stress, and apoptosis.


Autophagy; Endoplasmic reticulum stress; Oxidative stress; Rapamycin; Testis; Type 1 diabetes

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