动物造模,急性肾损伤 z-bio 2021-04-29 276

　　Objective: To study the effect of isoquinoxaline (ISO) on acute kidney injury (AKI) induced by cisplatin in mice, and to explore its potential regulatory mechanism.

　　Methods: 30C57BL/6 male mice were randomly divided into blank control group (NC group), model group (AKI group), low-dose isoquinoxaline (ISO-L) and high-dose (ISO-H) treatment groups Besartan... Positive control group (Irb group). Intraperitoneal injection of cisplatin (20 mg/kg) was used to establish an AKI model. During the intervention period, the NC group and AKI group received normal saline, the ISO-L group and ISO-H group received 7.5 mg/kg and 30 mg/kg isoquinoline, and the Irb group received 20 mg/kg. Gisar Besartan (kgir besartan). After 3 days of forced eating, the mice were sacrificed, and serum was collected to detect creatinine, urea nitrogen, HE and PAS staining to detect renal pathological changes, and perform immunohistochemistry and Western blotting for major inflammation analysis. (IL-6, IL-1β) and Smad3, NF-κB and other important protein activities, can detect the changes of inflammatory factors and long-chain non-coding Arid2-IR. Compared with the AKI group, isoflavone intervention can significantly improve mouse creatinine and urea nitrogen, and has a concentration-dependent adjustment; pathological staining results show that nephritis cell infiltration is reduced after drug intervention, which indicates that kidney damage is significantly improved; inflammatory factors , Smad3, NF-κB activity and long-chain non-coding Arid2-IR were all significantly down-regulated (P\u003c0.05). It has been shown that isoquinoxaline can inhibit the activation of Smad3/Arid2-IR/NF-κB axis.

　　Conclusion: Isoquinoxaline can effectively reduce kidney inflammation in AKI mice, and its mechanism may be related to the regulation of the Smad3/Arid2-IR/NF-κB axis.