The protective mechanism of salidroside modulating miR-199a-5p/TNFAIP8L2 on lipopolysaccharide-induced MLE-12 cells

红景天苷 脂多糖 细胞凋亡 TLR4型 免疫印迹 细胞因子 化学 肿瘤坏死因子α 细胞 分子生物学 炎症 污渍 HMGB1 免疫学 生物 药理学 生物化学 基因
作者
Yang Tan,Yong-fan Zou,Huang-bo Zhang,Xu Liu,Chuanyun Qian,Ming-wei Liu
出处
期刊:International Journal of Immunopathology and Pharmacology [SAGE Publishing]
卷期号:36: 039463202211327-039463202211327 被引量:4
标识
DOI:10.1177/03946320221132712
摘要

Salidroside is used for treating inflammation-based diseases; however, its molecular mechanism is unclear. In this study, we determined the protective role of salidroside on the endotoxin-induced damage caused to the mouse alveolar epithelial type II (MLE-12) cells and its underlying mechanism.An in vitro model for acute lung injury was constructed by inducing the MLE-12 cells using lipopolysaccharide (lipopolysaccharides, 1 mg/L). Then, The MTT assay was conducted to assess the survival rate of the MLE-12 cells in the different groups. After the treatment, apoptosis of MLE-12 cells was determined, and the mRNA and protein expression of miR-199a-5p, HMGB1, NF-kB65, TNFAIP8L2, p-IkB-α, and TLR4 was estimated by Western Blotting and RT-PCR. ELISA was also used to measure the concentration of inflammatory cytokine molecules IL-1β, IL-6, TNF-α, and IL-18 in the cell-free supernatant. Lastly, cell morphology was examined using the AO/EB technique.We showed that salidroside reduced the protein and gene expression of HMGB1, NF-kB65, miR-199a-5p, p-IkB-α, and TLR4, whereas it increased the gene and protein expression of TNFAIP8L2. Furthermore, it decreased the concentrations of cytokine molecules like IL-1β, IL-6, TNF-α, and IL-18 in the cell-free supernatant. MLE-12 also showed a lower apoptosis rate, higher survival rate, and better cell morphology.Salidroside significantly inhibited the LPS-induced MLE-12 cell damage. Our results suggest that this could be by reducing miR-199a-5p and enhancing TNFAIP8L2 expression.

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