Protective Effect of Artesunate on LPS-induced Acute Lung Injury by Anti-oxidant Through AKT/PI3K Pathway

被引:0
|
作者
Wang, Guo-quan [1 ,2 ]
Chao, Xu [1 ,2 ]
Li, Sha [2 ]
Yu, Lin-zhong [3 ]
Zhang, En-hu [1 ]
机构
[1] Shaanxi Univ Chinese Med, Xianyang 712046, Shaanxi, Peoples R China
[2] Shaanxi Univ Chinese Med, Affiliated Hosp 2, Xianyang 712046, Shaanxi, Peoples R China
[3] Southern Med Univ, Sch Tradit Chinese Med, Guangzhou 510515, Guangdong, Peoples R China
关键词
Artesunate; Acute lung injury; Anti-oxidant; AKT/PI3K pathway;
D O I
暂无
中图分类号
TP [自动化技术、计算机技术];
学科分类号
0812 ;
摘要
Oxidative stress are involved in the pathogenesis of acute lung injury (ALI). Accordingly, anti-inflammatory treatment is proposed to be a possible efficient therapeutic strategy for ALI. The aim of the study was to evaluate the antioxidant efficacy of Artesunate (Ar) on ALI induced by lipopolysaccharide (LPS) in mice and explore the underlying mechanism. BALB/c mice received Ar (2, 4 mg/kg) intraperitoneally 1h prior to the in intratracheal instillation of lipopolysaccharide (LPS) challenge. Malondialdehyde (MDA) was detected to evaluate the anti-oxidant efficacy of Artesunate. Content of Superoxide Dismutase (SOD) and Catalase (CAT) were assayed by enzyme linked immunosorbent assay (ELISA). Western blot was employed to determine the protein expression of P-PI3K, PI3K, P-AKT and AKT. The results showed the severity of lung injury was attenuated by Ar (40 mg/kg) and Dex (2 mg/kg) and the levels of MDA in Ar (20, 40 mg/kg) and Dex (2mg/kg) groups were obviously lower than those in LPS group. The treatment with Ar (20, 40 mg/kg) and Dex (2 mg/kg) remarkably increased the levels of SOD and CAT. The protein expressions of signaling showed the protein expressions of PI3Kand ATK significantly enhanced compared with those in LPS group after Areating with Ar (20 and 40 mg/kg) and Dex (2 mg/kg). In conclusion, this study revealed that Artesunate could exert protective effect of on LPS-induced acute lung injury by anti-oxidant through AKT/PI3K pathway.
引用
收藏
页码:529 / 534
页数:6
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