Protective effect and mechanism of Jinshuibao tablet on acute kidney injury induced by cisplatin in rats
10.11665/j.issn.1000-5048.20200112
- VernacularTitle:金水宝片对顺铂所致大鼠急性肾损伤的保护作用及机制
- Author:
Xuewu LIU
1
;
Zhiming ZHOU
;
Dejian JIANG
;
Li LONG
Author Information
1. 湖南省药物安全评价研究中心；新药药效与安全性评价湖南省重点实验室
- Publication Type:Journal Article
- Keywords:
Jinshuibao tablets;
cisplatin;
acute kidney injury;
mechanism
- From:
Journal of China Pharmaceutical University
2020;51(1):76-83
- CountryChina
- Language:Chinese
-
Abstract:
This study aimed to observe the therapeutic effect and mechanism of Jinshuibao tablet on acute renal injury induced by cisplatin. Acute renal injury models in SD rats were induced separately by single intraperitoneal injection of cisplatin(5 mg/kg)and intravenous injection for 5 consecutive days at a dosage of 2 mg/kg per day. The renal function and renal histopathological changes were observed in rat acute renal injury models after prevention and treatment with Jinshuibao tablet, respectively. The content of tumor necrosis factor(TNF-α)and reactive oxygen species(ROS), the activity of Caspase 3 and the expression of t-p38, p-p38, Bax and Bcl-2 in the kidneys were detected. The results showed that preventive and therapeutic administration of Jinshuibao tablets could both significantly inhibit the increase of the blood urea nitrogen(BUN)and creatinine(CRE), increase the creatinine clearance rate, reduce the contents of TNF-α and ROS, and decrease the activity of Caspase 3 in acute renal injury models induced by cisplatin. The renal histopathological results showed that Jinshuibao tablets could significantly reduce renal histopathology scores, ameliorate renal tubule degeneration and inflammatory infiltration. Western blot results showed that Jinshuibao tablets could significantly decrease the expression of t-p38 and p-p38, while increasing the Bcl-2/Bax ratio in the kidneys. These results suggested that preventive and therapeutic administration of Jinshuibao tablets could both improve renal function and pathological changes of renal tissue, which might be related to the inhibition of TNF-α and the ROS-p38 MAPK-Caspase3 pathway and thus inhibition of apoptosis.
