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@#[Abstract] Objective: To investigate the effect of metformin on the senescence-associated secretory phenotype (SASP) of doxorubicin-induced gastric cancer BGC823 cells. Methods: Human gastric cancer BGC823 cells were cultured in vitro and treated with doxorubicin at gradient concentrations (50, 100, 150 and 200 nmol/L). Cell senescence was detected by SA-β-gal staining, and SASP factor expression was detected by ELISA. The effects of metformin on cell senescence and SASP factor secretion induced by doxorubicin (100 nmol/L) were observed by adding gradient concentrations of metformin (0, 5, 10 and 20 mmol/L). Results: With the increase of doxorubicin concentration and treatment time, the senescence rate of gastric cancer BGC823 cells increased first and then decreased. At 96 h after 100 nmol/L doxorubicin treatment, the peak aging rate reached 68.7%, accompanied with significantly increased expressions of SASP factors IL-1a, IL-6, IL-8 and CXCL1. The proportion of senescent cells was (55.2±1.9)%, (48.7±2.2)% and (40.8±2.3)% respectively under the effects of 5, 10 and 20 mmol/L metformin, which was significantly lower than that in the non-metformin treatment group (P< 0.01). At the same time, with the increase of metformin concentration, the production of SASP factors IL-1α, IL-6, IL-8 and CXCL1 showed a gradient decline. Compared with the non-metformin treatment group, IL-6 and IL-8 decreased significantly under the effect of metformin above 10 mmol/L (P<0.05 or P<0.01), while IL-1α and CXCL1 decreased significantly under the effect of 20 mmol/L metformin (all P<0.05). Conclusion: Metformin can inhibit the senescence and SASP production of gastric cancer cells induced by doxorubicin.
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@#[Abstract] Objective: To investigate the effect of Xihuang (XH) extract on the proliferation of gastric cancer SGC-7901 cells and its underlying mechanism. Methods: Gastric cancer cell line SGC-7901 was conventionally cultured. CCK-8 assay and flow cytometry were used to detect the effect of different concentrations of XH extracts (3.2, 6.4, 12.8, and 25.6 mg/ml) on proliferation and apoptosis of SGC-7901 cells after treatment for different time periods (24, 48, and 72 h); The effect of different concentrations of XH extracts on the mRNA expression of apoptosis-related genes (Bax and Bcl-2) was detected by qPCR; Western blotting was used to detect the effect of XH extracts on the expression of apoptosis-associated proteins (caspase 3, caspase 9, Bax and Bcl-2). Results: XH extracts (3.2, 6.4, 12.8, and 25.6 mg/ml) could effectively inhibit proliferation of gastric cancer SGC-7901 cells (P<0.05 or P<0.01) in a concentration-depend manner (P<0.01). XH extract could significantly up-regulate Bax mRNAand down-regulate Bcl-2 mRNAexpression (P<0.05 or P <0.01); Meanwhile, XH extract ouldincrease protein expressions of caspase 3, caspase 9, Bax but reduce Bcl-2 protein expression (P< 0.05 or P<0.01). Conclusion: XH extract can inhibit the proliferation of gastric cancer SGC-7901 cells by triggering apoptosis, which may become a potential method of adjuvant treatment of gastric cancer.