茶黄素调节PI3K/Akt/mTOR信号通路对A549细胞增殖凋亡及自噬的影响

doi:10.3969/j.issn.1006-6233.2024.09.011

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Abstract Objective: To investigate the effects of theaflavin on A549 cell proliferation, apoptosis, and autophagy by regulating the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway.Methods: The proliferation rate of A549 cells was measured after intervention with 0, 2.5, 5, 10, 20, 40, 80, and 160 μmol/L theaflavin, and the appropriate concentration of action was screened. A549 cells were separated into control group, low theaflavin group (20 μmol/L theaflavin), medium theaflavin group (40 μmol/L theaflavin), high theaflavin group (80 μmol/L theaflavin), and high theaflavin+740Y-P group (80 μmol/L theaflavin+30 μmol/L PI3K/Akt/mTOR signaling pathway activator 740Y-P). CCK-8 method and plate colony formation experiment were applied to determine the proliferation of A549 cells. Flow cytometry and MDC methods were applied to determine apoptosis and autophagic vacuole formation in A549 cells, respectively. Western blot was applied to determine the expression of PI3K/Akt/mTOR signaling pathway proteins and autophagy proteins in A549 cells.Results: Compared with 0 μmol/L of theaflavin, 2.5, 5, 10, 20, 40, 80, and 160 μmol/L of theaflavin can inhibit the proliferation of A549 cells. The IC50 value of theaflavin on A549 cells was calculated to be 36.72 μmol/L. Compared with the control group, the proliferation rate, colony formation rate, p-PI3K/PI3K, p-Akt/Akt, and p-mTOR/mTOR of A549 cells in the low theaflavin group, medium theaflavin group, and high theaflavin group all reduced, the apoptosis rate, relative content of autophagic vacuoles, LC3II/LC3I, and Beclin-1 protein expression all increased, and all showed dose-dependent changes in theaflavin (P<0.05). Compared with the high theaflavin group, the proliferation rate, colony formation rate, p-PI3K/PI3K, p-Akt/Akt, and p-mTOR/mTOR of A549 cells in the high theaflavin+740Y-P group all increased, the apoptosis rate, relative content of autophagic vacuoles, LC3II/LC3I, and Beclin-1 protein expression all reduced (P<0.05).Conclusion: Theaflavin can induce protective autophagy by inhibiting the activation of the PI3K/Akt/mTOR signaling pathway, thereby promoting apoptosis and inhibiting the proliferation of lung cancer cells.

Key words： Theaflavin Phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin signaling pathway Autophagy Lung cancer

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	DUAN Xinglong
	ZHANG Hua

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DUAN Xinglong,ZHANG Hua. Effects of Theaflavin on Proliferation Apoptosis and Autophagy of A549 Cell by Regulating the PI3K/Akt/mTOR Signaling Pathway[J]. HeBei Med, 2024, 30(9): 1473-1477.

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http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2024.09.011 OR http://www.hbyxzzs.cn/EN/Y2024/V30/I9/1473

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