Zhao Lingling, Gu Qianru, Xiang Lanting, Dong Xidan, Li Huimin, Ni Jinyao, Wan Li, Cai Guoping, Chen Guorong
Department of Pathology, Zhejiang Provincial Hospital of TCM, Hangzhou.
Department of Pathology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, People's Republic of China.
Ther Clin Risk Manag. 2017 Aug 28;13:1099-1105. doi: 10.2147/TCRM.S141738. eCollection 2017.
The present study was designed to examine the damage caused by high-fat diet and streptozotocin-induced diabetes on the testis of rats and the effects of curcumin against oxidative stress and apoptosis from high-fat diet and diabetes.
Diabetes was induced by intraperitoneal injection of streptozotocin (30 mg/kg in 0.1 M sodium citrate buffer, pH 4.5) in obese rats. The rats in the obese and diabetic groups were treated with a daily dose of curcumin by intragastric intubation (100 mg/kg body weight) for 8 weeks. Testis tissue sections were stained with hematoxylin-eosin, and apoptosis was identified in situ by using terminal deoxynucleotidyl transferase dUTP nick end labeling.
Curcumin treatment improved the histological appearance of the testis and significantly reduced the apoptosis level in the testicular cells of the obese and the diabetic rats. The expression of proliferating cell nuclear antigen (PCNA) was restored in the testis tissues of diabetic rats at the end of curcumin treatment. Molecular analysis demonstrated that curcumin treatment significantly and simultaneously decreased Bax and increased Bcl-2 expressions, therefore elevating the ratio of Bcl-2/Bax. Furthermore, curcumin treatment significantly decreased malondialdehyde (MDA) and increased superoxide dismutase (SOD) levels in testis tissue samples of the diabetic rats.
Curcumin treatment preserved the morphology of testes; restored the expression of PCNA, MDA, and SOD; and inhibited testicular cell death in diabetic rats. The capability of curcumin in inhibiting oxidative stress and modulating the Bax/Bcl-2-mediated cell death pathway reveals its potential as a therapeutic agent against diabetes.
本研究旨在检测高脂饮食和链脲佐菌素诱导的糖尿病对大鼠睾丸造成的损伤,以及姜黄素对高脂饮食和糖尿病所致氧化应激和细胞凋亡的影响。
通过腹腔注射链脲佐菌素(30mg/kg,溶于0.1M柠檬酸钠缓冲液,pH4.5)诱导肥胖大鼠患糖尿病。肥胖和糖尿病组大鼠通过灌胃给予每日剂量的姜黄素(100mg/kg体重),持续8周。睾丸组织切片用苏木精-伊红染色,采用末端脱氧核苷酸转移酶dUTP缺口末端标记法原位鉴定细胞凋亡。
姜黄素治疗改善了睾丸的组织学外观,并显著降低了肥胖和糖尿病大鼠睾丸细胞的凋亡水平。姜黄素治疗结束时,糖尿病大鼠睾丸组织中增殖细胞核抗原(PCNA)的表达得以恢复。分子分析表明,姜黄素治疗显著且同时降低了Bax的表达并增加了Bcl-2的表达,从而提高了Bcl-2/Bax的比值。此外,姜黄素治疗显著降低了糖尿病大鼠睾丸组织样本中的丙二醛(MDA)水平,并提高了超氧化物歧化酶(SOD)水平。
姜黄素治疗保留了糖尿病大鼠睾丸的形态;恢复了PCNA、MDA和SOD的表达;并抑制了睾丸细胞死亡。姜黄素抑制氧化应激和调节Bax/Bcl-2介导的细胞死亡途径的能力揭示了其作为糖尿病治疗药物的潜力。