Wei Zhengkai, He Xuexiu, Kou Jinhua, Wang Jingjing, Chen Libin, Yao Minjun, Zhou Ershun, Fu Yunhe, Guo Changming, Yang Zhengtao
College of Veterinary Medicine, Jilin University, Jilin, Changchun 130062, People's Republic of China.
College of Veterinary Medicine, Jilin University, Jilin, Changchun 130062, People's Republic of China.
Int Immunopharmacol. 2015 Sep;28(1):500-6. doi: 10.1016/j.intimp.2015.07.009. Epub 2015 Jul 25.
In this study, we investigated the renoprotective effects of morin on cisplatin-induced kidney injury in mice. Serum creatinine and blood urea nitrogen (BUN) levels, glutathione peroxidase (GSH-PX) and superoxide dismutase (SOD) activities were determined according to the corresponding kits. The mRNA levels of TNF-α and IL-1β in kidney tissues were measured by quantitative real-time PCR (qRT-PCR). The activities of cytochrome P450 2E1 (CYP2E1), nuclear factor kappa B (NF-κB) p65, P38 mitogen-activated protein kinase (MAPK), Bax, p53 and cleaved caspase 3 were evaluated by western blotting. The results showed that the model of cisplatin-induced kidney injury was successfully replicated, and morin significantly attenuated histopathological changes and decreased the levels of TNF-α and IL-1β in the kidneys. In addition, morin attenuated the activation of CYP2E1, phospho-NF-κB p65, phospho-P38 MAPK, Bax, phospho-p53 and cleaved caspase 3 in CP-induced kidney injury. In conclusion, these results indicated that the renoprotective mechanisms of morin may be attributed to the suppression of oxidative stress, inflammation and apoptosis in CP-induced kidney injury.
在本研究中，我们调查了桑色素对顺铂诱导的小鼠肾损伤的肾脏保护作用。根据相应试剂盒测定血清肌酐和血尿素氮（BUN）水平、谷胱甘肽过氧化物酶（GSH-PX）和超氧化物歧化酶（SOD）活性。通过定量实时PCR（qRT-PCR）测量肾组织中TNF-α和IL-1β的mRNA水平。通过蛋白质印迹法评估细胞色素P450 2E1（CYP2E1）、核因子κB（NF-κB）p65、P38丝裂原活化蛋白激酶（MAPK）、Bax、p53和裂解的半胱天冬酶3的活性。结果表明，成功复制了顺铂诱导的肾损伤模型，桑色素显著减轻了组织病理学变化，并降低了肾脏中TNF-α和IL-1β的水平。此外，桑色素减弱了顺铂诱导的肾损伤中CYP2E1、磷酸化-NF-κB p65、磷酸化-P38 MAPK、Bax、磷酸化-p53和裂解的半胱天冬酶3的激活。总之，这些结果表明，桑色素的肾脏保护机制可能归因于对顺铂诱导的肾损伤中氧化应激、炎症和细胞凋亡的抑制。
