丙泊酚通过激活Nrf2/HO-1信号通路减轻脓毒症诱导的急性肺损伤
Propofol alleviates sepsis induced acute lung injury by activating the Nrf2/HO-1 signaling pathway
缪文禹 1毛舜 2佟昌慈2
作者信息
- 1. 辽宁省金秋医院手术麻醉科,辽宁沈阳 110016
- 2. 沈阳医学院树入国际学院,辽宁沈阳 110031
- 折叠
摘要
目的 探讨丙泊酚是否通过调控Nrf2/HO-1信号通路减轻脓毒症诱导的急性肺损伤.方法 50只健康雄性C57BL/6小鼠随机分为对照组(10只)、模型组(20只)和丙泊酚组(20只),通过盲肠结扎穿孔(CLP)小鼠模型建立脓毒症诱导的急性肺损伤.肺湿干重比评价肺水肿程度;HE染色评价小鼠肺组织病理情况;ELISA检测小鼠血清炎症因子IL-1β、IL-6和TNF-α的水平,以及肺组织MPO、MDA、SOD和GSH-Px的水平;Western blot实验检测大鼠肺组织NF-κB、Nrf2与HO-1的蛋白表达情况.结果 丙泊酚会缓解CLP导致的小鼠肺水肿以及小鼠肺组织病理改变,降低血清炎症因子IL-1β、IL-6和TNF-α的水平(P＜0.05);降低肺组织MPO和MDA的表达水平,上调SOD和GSH-Px的达水平(P＜0.05);降低大鼠肺组织NF-κB的表达,上调Nrf2与HO-1的蛋白表达(P＜0.05).结论 丙泊酚可能通过激活Nrf2/HO-1信号通路减轻脓毒症导致的肺组织损伤.
Abstract
Objective To investigate whether propofol alleviates sepsis-induced acute lung injury by regulating the Nrf2/HO-1 signaling pathway.Methods Fifty healthy male C57BL/6 mice were randomly divided into control group(n=10),model group(n=20)and propofol group(n=20).Sepsis-induced acute lung injury was established by cecal ligation and puncture(CLP).The degree of pulmonary edema was evaluated by the ratio of lung wet weight to dry weight;the pathological changes of lung tissue were evaluated by HE staining;the levels of IL-1β,IL-6 and TNF-α in serum and the levels of MPO,MDA,SOD and GSH-Px in lung tissue were detected by ELISA;The protein expressions of NF-κB,Nrf2 and HO-1 were detected by Western blot.Result Propofol alleviated the pulmonary edema and pathological changes of lung tissue in mice induced by CLP,decreased the levels of serum inflammatory cytokines IL-1β,IL-6 and TNF-α(P＜0.05),decreased the expression levels of MPO and MDA in lung tissue,and increased the levels of SOD and GSH-Px(P＜0.05).The expression of Nrf2 and HO-1 in lung tissue were up-regulated,while the expression of NF-κB was down-regulated(P＜0.05).Conclusion Propofol alleviates sepsis induced acute lung injury by upregulating the Nrf2/HO-1 signaling pathway.
关键词
脓毒症/急性肺损伤/丙泊酚/Nrf2/HO-1信号通路Key words
sepsis/acute lung injury/propofol/Nrf2/HO-1引用本文复制引用
出版年
2024
NETL
NSTL
万方数据