目的 探討紅景天苷對(duì)順鉑誘導(dǎo)小鼠急性腎損傷的保護(hù)作用及機(jī)制。方法 將SPF級(jí)昆明小鼠隨機(jī)分為對(duì)照組、模型組、紅景天苷組、順鉑＋紅景天苷組，每組7只。紅景天苷組和順鉑＋紅景天苷組小鼠ig 150 mg/kg紅景天苷2周，其余組ig等量生理鹽水，自第11天起，模型組和順鉑＋紅景天苷組ip 10 mg/kg順鉑誘導(dǎo)小鼠急性腎損傷模型，其余組ip等量生理鹽水。各組檢測(cè)血清肌酐（Scr）和尿素氮（BUN）水平，腎臟病理組織學(xué)變化，小鼠Toll-樣受體4（TLR4）、髓樣分化因子88（Myd88）、核因子κB（NF-κB）mRNA及蛋白表達(dá)。結(jié)果 與順鉑組比較，順鉑＋紅景天苷組小鼠Scr與BUN水平顯著降低（P＜0.05），小鼠腎臟損傷明顯改善，TLR4、Myd88和NF-κB mRNA及蛋白表達(dá)顯著降低（P＜0.05）。結(jié)論 紅景天苷對(duì)順鉑導(dǎo)致的急性腎損傷具有保護(hù)作用，其機(jī)制可能與抑制TLR4/Myd88/NF-κB通路的激活有關(guān)。

Objective To explore the protective effect and mechanism of salidroside against cisplatin-induced acute kidney injury in mice. Methods SPF Kunming mice were randomly divided into control group, model group, salidroside group, cisplatin + salidroside group, with 7 mice in each group. Cisplatin and cisplatin + salidroside groups were ig 150 mg/kg salidroside for 2 weeks, and the remaining groups were treated with equivalent amounts of saline. Since day 11, model and cisplatin + salidroside groups groups received 10 mg/kg cisplatin-inducedacute kidney injury model, and the remaining groups were given equal amounts of saline. Scr and levels, pathological histological changes in kidney, TLR4, Myd88 and NF-κB mRNA and protein expression in mice were measured. Results Compared with cisplatin group, Scr and BUN levels were significantly decreased (P < 0.05), kidney injury were improved, and the mRNA and protein expression of TLR4, Myd 88, NF- κB were significantly decreased (P < 0.05). Conclusion Salidroside has a protective effect on acute kidney injury caused by cisplatin, and the mechanism may be related to the inhibition of the activation of the TLR4/Myd88/NF-κB pathway.

R285.5

湖南省大學(xué)生創(chuàng)新創(chuàng)業(yè)訓(xùn)練計(jì)劃項(xiàng)目（S202310531044）