RTA408通过激活Nrf2减轻小鼠支原体肺炎肺损伤

RTA-408 alleviates Mycoplasma pneumonia in mice via activating Nrf2

目的探索RTA-408对肺炎支原体肺炎小鼠肺损伤的作用及可能机制。方法BALB/c小鼠40只随机分为空白对照组(control)、肺炎支原体肺炎组(MP)、RTA-408治疗组(RTA,100μg/kg)和ML-385组(ML,30mg/kg),每组10只。荧光定量PCR检测各组小鼠病原载量;HE染色观察各组小鼠肺组织形态学变化;ELISA试剂盒检测各组小鼠肺组织氧化应激指标;免疫荧光检测各组小鼠肺组织ROS表达;Western blot检测各组小鼠肺组织Nrf2的表达情况。结果RTA-408可以有效降低支原体肺炎小鼠病原载量,改善肺组织损伤形态;减少ROS释放,显著降低氧化应激水平。RTA能够上调支原体肺炎小鼠肺组织Nrf2蛋白表达,且Nrf2抑制剂能够逆转RTA-408对肺炎损伤的保护作用。结论RTA-408能够减轻支原体肺炎小鼠肺损,其作用机制可能与激活Nrf2有关。

Objective To explore the effect and possible mechanism of RTA-408 on lung injury in mice with Mycoplasma pneumoniae pneumonia.Methods Forty BALB/c mice were randomly divided into blank control group(control),Mycoplasma pneumoniae pneumonia group(MP)and RTA-408 treatment group(RTA,100μg/kg)and ML-385 group(ML,30 mg/kg),with 10 rats in each group.The pathogen load of mice in each group was detected by fluorescence quantitative PCR.HE staining was used to observe the morphological changes of lung tissue in each group.The indexes of oxidative stress in lung tissue of mice in each group were detected by ELISA.The expression of ROS in lung tissue of mice in each group was detected by immunofluorescence.The expression of Nrf2 in lung tissue of mice in each group was detected by Western blot.Results RTA can effectively reduce the pathogen load of Mycoplasma pneumonia mice,improve the morphology of lung tissue injury,reduce ROS release and the level of oxidative stress.RTA-408 can up-regulate the expression of Nrf2 in lung tissue of Mycoplasma pneumonia mice,and Nrf2 inhibitor can reverse the protective effect of RTA-408 on pneumonia injury.Conclusion RTA-408 can reduce lung damage in mice with Mycoplasma pneumonia,and its mechanism may be related to the activation of Nrf2.