The protective effect of recombinant globular adiponectin on testis by modulating autophagy, endoplasmic reticulum stress and oxidative stress in streptozotocin-induced diabetic mice

Abstract

This study was to investigate whether recombinant globular adiponectin produced its protective effect on the testis of diabetic mice by modulating autophagy, endoplasmic reticulum stress and oxidative stress. Male mice were randomly divided into control, diabetic, diabetic treated with low and high dose of adiponectin. Mice were killed at the termination after 4 weeks and 8 weeks of adiponectin treatment. Serum levels of glucose, lipids, testosterone, insulin, LH and FSH were measured. The protein expression of glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), Caspase12, Beclin1, microtubule-associated protein light chain 3 (LC3) and p62 was determined by western blotting. The mRNA expression of adiponectin receptor 1 (AdipoR1), p22phox, p47phox, nuclear factor erythroid2-related factor 2 (Nrf2), NAD(P)H-quinone oxidoreductase 1(NQO1), heme oxygenase-1 (HO-1) and superoxide dismutase (SOD) were determined by real-time fluorescence quantitative PCR. The testicular weight, the sperm number and motility, and the serum levels of testosterone and insulin were significantly decreased in diabetic mice (P < 0.05). The expression of Beclin1, LC3, Nrf2, NQO1, HO-1, SOD and AdipoR1 were significantly decreased (P < 0.05), while the expression of GRP78, CHOP, Caspase12, p62, p22phox and p47phox were notably increased in the testes of diabetic mice (P < 0.05). Adiponectin treatment significantly reversed the above-mentioned changes in the testes of diabetic mice, some of which were dose- and time-dependent (P < 0.05). These data suggested that recombinant globular adiponectin may produce the protective effect on the testes of diabetic mice by inducing autophagy and inhibiting ER stress and oxidative stress.