动物造模,急性肾损伤小鼠炎症 z-bio 2021-02-19 310

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

　　Methods: C57BL/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 isquiline, respectively, and the Irb group received 20 mg/kg. Be given. 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 pathological changes in the kidneys. Immunohistochemistry and Western blotting were used for detection. Real-time PCR is an inflammatory factor (IL-6, IL-1β) and the activity of important proteins such as Smad3 and NF-κB. It can detect changes in inflammatory factors and long-chain non-coding Arid2-IR. Compared with the AKI group, the isoflavone intervention can significantly improve the creatinine and urea nitrogen of the mice (P\u003c0.05), and it can be adjusted in a concentration-dependent manner; the pathological staining result is that the drug intervention shows that the nephritis cell infiltration is reduced. After that, kidney damage was significantly improved; inflammatory factors, Smad3, NF-κB activity, and long-chain non-coding Arid2-IR expression were significantly down-regulated (P\u003c0.05), and isoflavones activated the 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.