Protective effects of betaine on diabetic induced disruption of the male mice blood-testis barrier by regulating oxidative stress-mediated p38 MAPK pathways

Biomedicine & Pharmacotherapy

Ping Liu¹  Ning Liu²  Wen-Jin Zhang²  Ya-Ping Jiang²  Jia-Mei Yang²  Rui-Juan Ye²  Ping Zheng²  Lin Ma³  Jian-Guo Niu³  Jian-Qiang Yu⁴ 

[1]Corresponding author.

[2]Department of Pharmacology, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, 750004, PR China

[3]Ningxia Key Laboratory of Craniocerebral Diseases of Ningxia Hui Autonomous Region, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, 750004, PR China

[4]Ningxia Medical University General Hospital, Yinchuan, Ningxia Hui Autonomous Region, 750004, PR China

关键词: Protective effects;    Betaine;    Diabetic mice;    Blood testis barrier dysfunction;    Oxidative stress/p38 MAPK;   

DOI  :  

来源: DOAJ

【 摘 要 】

Background: Blood-testis barrier (BTB) impairments is one of the major secondary complications of diabetes. Betaine (BET) is the important active ingredients isolated from Lycium barbarum, which exhibits numerous pharmacological activities such as antioxidant, anti-diabetic, and anti-inflammatory effects. This study aimed to establish whether BET contributes to the recovery from BTB dysfunction in streptozotocin (STZ) induced diabetic mice. Methods: BET (200, 400, 800 mg/kg) was orally administered to diabetic mice for 8 weeks. Testis tissues were collected for histopathological and biochemical analysis, the reproductive organ weight was estimated. Antioxidant enzyme activity and BTB associated protein expressions were determined with their corresponding assay kits and western blot analysis. The results revealed that BET significantly improved the weight of the reproductive organs and testicular morphology in diabetic mice. Furthermore, reactive oxygen species (ROS) and malondialdehyde (MDA) levels were significantly reduced, and the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH), markedly increased in the testicular tissue after SAL treatment. In addition, our data also showed a marked down-regulated the expressions of p38 MAPK phosphorylation and up-regulation the protein expressions of ZO-1, Occludin, Claudin-11, N-cadherin, and Connexin-43 after BET administration compared with the diabetic group. In conclusion, these results demonstrated that BET exerts protective effects on diabetes-induced BTB dysfunction, which may be through regulating oxidative stress-mediated p38 MAPK pathways.

【 授权许可】

Unknown