Research on Mechanism of Qingfei Fang Regulating PPARγ/NF-κB Signaling Pathway to Inhibit Inflammatory Oxidative Stress of Human Bronchial Epithelioid Cells
- VernacularTitle:清肺方上调PPARγ/NF-κB通路抑制人气道上皮细胞炎症氧化应激反应的机制研究
- Author:
Zhe ZHE
1
;
Yongning SUN
1
Author Information
- Publication Type:Journal Article
- Keywords: Qingfei Fang; PPARγ/NF-κB signaling pathway; Human bronchial epithelioid cells; Inflammatory response; Oxidative stress
- From: World Science and Technology-Modernization of Traditional Chinese Medicine 2025;27(8):2119-2131
- CountryChina
- Language:Chinese
- Abstract: Objective To investigate the mechanism of Qingfei Fang(QF)protecting human bronchial epithelioid cells 16(16HBE).Methods The potential targets of QF on cellular inflammation by network and pharmacology analysis were identified.The effects of different concentrations and exposure times of QF on the relative viability of LPS induced 16HBE cells were measured by CCK8.16HBE cells were divided into control group,model group,QF group,and shPPARγ group.The control group was received no treatment,the model group was treated with 200 ng·mL-1 LPS for 24 h,the QF group was treated with 200 ng·mL-1 LPS and 40 ng·mL-1 QF for 24 h,and the shPPARγ group was treated with 40 ng·mL-1 QF for 4 h in the 16HBE-M-4 cell line before being treated with 200 ng·mL-1 LPS for 4 h.The levels of interleukin-6,interleukin-10,tumor necrosis factor-α,malondialdehyde,and superoxide dismutasein the cell culture supernatant were detected by ELISA.Polymerase chain reaction was applied to detect the mRNA levels of NF-κB p50 and p65 in cell supernatants.Western blot was applied to detect the protein expression of NF-κB p65 in 16HBE.Results Sanggenon D and Coptis chinensis bind to target protein PPARγ.Subsequent cell experiments were carried out with the concentration of 40 ng·mL-1 Qingfei Fang.Compared to the control group,cell viability reduced,levels of IL-6,TNF-αand MDA increased,and levels of IL-10 and SOD decreased significantly(P<0.05)in the model group.The levels of NF-κB p50 and p65 mRNA also increased significantly(P<0.05),indicating successful induction of an inflammatory phenotype in the model group.Compared to the model group,the levels of IL-6,TNF-α,and NF-κB in the cell culture supernatant reduced in the QF group,while the levels of IL-10 and SOD increased significantly(P<0.05).After lentivirus-mediated shPPARγ transfection,the ability of QF to reduce IL-6,TNF-α,and NF-κB p65 levels and to increase IL-10 and SOD levels were inhibited(P<0.05).Conclusion QF may exert a protective effect on 16HBE cells by upregulating PPARγ to inhibit NF-κB pathway-mediated inflammatory response and oxidative stress.
