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

氧化应激 超氧化物歧化酶 丙二醛 链脲佐菌素 内分泌学 内科学 活性氧 过氧化氢酶 免疫印迹 抗氧化剂 糖尿病 谷胱甘肽过氧化物酶 谷胱甘肽 p38丝裂原活化蛋白激酶 化学 MAPK/ERK通路 药理学 生物 医学 激酶 生物化学 基因
作者
Yaping Jiang,Jiamei Yang,Rui-Juan Ye,Ning Liu,Wenjin Zhang,Lin Ma,Ping Zheng,Jianguo Niu,Ping Liu,Jianqiang Yu
出处
期刊:Biomedicine & Pharmacotherapy [Elsevier BV]
卷期号:120: 109474-109474 被引量:64
标识
DOI:10.1016/j.biopha.2019.109474
摘要

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.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.
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