急性肾损伤小鼠炎症,异甘草素 z-bo 2020-10-22 371

　　Objective To study the effect of isoliquiritin (ISO) on cisplatin-induced acute kidney injury (AKI) in mice and explore the underlying regulatory mechanism.

　　Methods Thirty C57BL/6 male mice were randomly divided into blank control group (NC group), model group (AKI group), low-dose (ISO-L) and high-dose (ISO-H) treatment groups of isoliquiritin. Besartan positive control group (Irb group). The AKI model was established by a single intraperitoneal injection of cisplatin (20 mg/kg). During the intervention, the NC group and AKI group were given normal saline, while the ISO-L group and ISO-H group were given isoliquiritin 7.5 mg/kg and 30 mg/kg, respectively, and the Irb group was given 20 mg/kg irbesartan. The mice were sacrificed after 3 days of intragastric administration. Serum was collected to detect creatinine, urea nitrogen, HE and PAS staining to detect renal pathological changes, immunohistochemistry and western blotting to detect key inflammation factors (IL-6, IL-1β) and Smad3, NF-κB and other key protein activity, Real-time PCR detects the changes of inflammatory factors and long-chain non-coding Arid2-IR.

　　Results Compared with the AKI group, the isoliquiritin intervention can significantly improve mouse creatinine and urea nitrogen (P<0.05), and it is concentration-dependently regulated; the pathological staining results show that the nephritis cell infiltration is reduced after drug intervention, and the kidney injury is obvious Improvement; and the expression of inflammatory factors, Smad3, NF-κB activity, and long-chain non-coding Arid2-IR were all significantly down-regulated (P<0.05), indicating that isoliquiritin can inhibit Smad3/Arid2-IR/NF-κB axis The activation.

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