Guben Qingfei decoction attenuates LPS-induced acute lung injury by modulating the TLR4/NF-κB and Keap1/Nrf2 signaling pathways

被引:10
作者
Zeng, Ziyuan [2 ]
Fu, Yuchen [1 ]
Li, Minfang [3 ]
Shi, Yuanyuan [1 ,2 ]
Ding, Qi [2 ]
Chen, Sheng [3 ]
机构
[1] Beijing Univ Chinese Med, Sch Life Sci, Beijing, Peoples R China
[2] Beijing Univ Chinese Med, Shenzhen Res Inst, 1201,East Block A,16 Lanjingzhong Rd, Shenzhen 518118, Guangdong, Peoples R China
[3] Shenzhen Tradit Chinese Med Hosp, 1 Fuhua Rd, Shenzhen 518033, Guangdong, Peoples R China
关键词
Acute lung injury; Guben Qingfei decoction; Anti-Inflammatory; Anti-Oxidative; Traditional Chinese Medicine; NF-KAPPA-B; OXIDATIVE STRESS; INFLAMMATION; MICE; PATHOGENESIS;
D O I
10.1016/j.jep.2023.117674
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Ethnopharmacological relevance Acute lung injury (ALI) is a life-threatening and widespread disease, with exceptionally high morbidity and mortality rates. Unfortunately, effective drugs for ALI treatment are currently lacking. Guben Qingfei decoction (GBQF) is a Chinese herbal compound known for its efficacy in treating viral pneumonia, yet the precise underlying mechanisms remain unknown. Aim of the study: This study aimed to validate the mitigating effect of GBQF on ALI and to further investigate its mechanism. Materials and methods An ALI mice model was established by infusing LPS into the endotracheal tube. The effects of GBQF on ALI were investigated by measuring lung W/D; MPO; BALF total protein concentration; total number of cells; TNF-alpha, IL-1 beta, and IL-6 levels; pathological changes in lung tissue, and oxidation products. Immunohistochemistry and Western Blotting were performed to verify the underlying mechanisms. MH-S and BEAS-2B cells were induced by LPS, and the effects of GBQF were confirmed by RT-PCR and immunofluorescence. Results GBQF significantly reduced LPS-induced ALI in mice, improved lung inflammation, reduced the production of oxidative products, increased the activity of antioxidant enzymes, and reduced the degree of lung tissue damage. GBQF prevents MH-S cells from releasing inflammatory factors and reduces oxidative damage to BEAS-2B cells. In vivo studies have delved deeper into the mechanism of action of GBQF, revealing its correlation with the TLR4/NF-kappa B and Keap1/Nrf2 pathways. Conclusions Our study demonstrates that GBQF is an effective treatment for ALI, providing a new perspective on medication development for ALI treatment.
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页数:11
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