Background and Objective:
This study investigated whether rapamycin has a protective
effect on the testis of diabetic rats by regulating autophagy, endoplasmic reticulum stress, and oxidative
stress.
Methods:
Thirty male Sprague-Dawley rats were randomly divided into three groups: control, diabetic,
and diabetic treated with rapamycin, which received gavage of rapamycin (2mg.kg-1.d-1) 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.
Results:
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).
Conclusion:
Rapamycin appears to produce a 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.
Sestrin2 suppression aggravates oxidative stress and apoptosis in endothelial cells subjected to pharmacologically induced endoplasmic reticulum stress
