Abstract 【Objective】 To investigate the protective effect of emodin on alveolar epithelial cell injury induced by Streptococcus pneumoniae and its mechanism. 【Methods】A549 alveolar epithelial cells were randomly divided into control group, model group and 20 μg/mL group, 40 μg/mL group, 80 μg/mL group, 160 μg/mL group, the cells in the control group were cultured routinely, and the cells in the other groups were infected by Streptococcus pneumoniae; 20 μg/mL group, 40 μg/mL group, 80 μg/mL group, 160 μg/mL group cells were added with different concentrations of emodin (20 μg/mL,40 μg/mL,80 μg/mL,160 μg/mL). The proliferation of A549 cells was detected by MTT; The apoptosis rate was detected by flow cytometry; Level of interleukin-6 (IL-6) and tumor necrosis factor-α(TNF-α)was detected by enzyme linked immunosorbent assay (ELISA) ; In A549 cells, B cell lymphoma / leukemia-2 (Bcl-2), Bcl-2 associated X protein (Bax), cleaved caspase containing cysteine-3(Cleaved Caspase-3),β-catenin and the protein levels of Cyclin D1 were detected by Western blot. 【Results】 Compared with the control group,the protein levels of the proliferative activity, Bcl-2, β-catenin and cyclin D1 decreased (P<0.05); The levels of apoptosis rate, IL-6 and TNF-α, Bax and cleared Caspase-3 protein increased (P<0.05); Different concentrations of emodin could promote the proliferation of A549 cells infected by Streptococcus pneumoniae (P<0.05), inhibit its apoptosis (P<0.05), and reduce IL-6 and TNF-α level (P<0.05), increase Bcl-2 protein level (P<0.05), decrease Bax and Cleaved Caspase-3 protein level (P<0.05) and increase protein levels of β-catenin and cyclin D1 (P<0.05). 【Conclusion】 Emodin may regulate Wnt/β-catenin signaling pathway, promote the proliferation of alveolar epithelial cells infected by Streptococcus pneumoniae and inhibit their apoptosis.
SUN Jian-rong,ZHAO Jing,LIU Wen-lin. Protective Effect of Emodin on Alveolar Epithelial Cell Injury Induced by Streptococcus Pneumoniae and its Mechanism[J]. JOURNAL OF CLINICAL RESEARCH, 2022, 39(7): 1006-1009.
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2022, Vol. 39 
