Wang Chun-Mei, Qi Wen-Jing, Ren Yan-Jiao, Sheng Guang-Yao
Children's Hospital, First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Zhongguo Dang Dai Er Ke Za Zhi. 2022 Jul 15;24(7):821-825. doi: 10.7499/j.issn.1008-8830.2202078.
To explore the effect of polydatin on the proliferation and apoptosis of acute monocytic leukemia cell line THP-1 and the possible mechanism.
After THP-1 cells were treated with polydatin at gradient concentrations for 24 hours and 48 hours, their proliferation was determined by CCK-8 assay, and half maximal inhibitory concentration (IC50) was calculated. Logarithmically growing THP-1 cells were divided into two groups, a polydatin treatment group (treated with IC50 of polydatin) and a blank control group (treated without polydatin solution), and incubated for 48 hours. Cell apoptosis and cell cycle were measured by flow cytometry. The expression levels of PI3K, AKT, p-AKT, mTOR, p-mTOR, p70 S6K, and p-p70 S6K proteins were measured by Western blotting.
After treatment with polydatin, the proliferation of THP-1 cells was strongly inhibited, and the IC50 at 48 hours was 1 800 μmol/L. After treatment with 1 800 μmol/L polydatin solution for 48 hours, the apoptosis rate of THP-1 cells increased significantly compared with the blank control group (<0.05). The cell cycle was arrested in the G/G and S phases, with a significantly increased proportion of cells in the G/G phase and a significantly decreased proportion of cells in the S phase, as compared with the blank control group (<0.05). The expression levels of PI3K, AKT, p-AKT, mTOR, p-mTOR, p70 S6K, and p-p70 S6K proteins decreased significantly compared with the blank control group (<0.05).
Polydatin can effectively inhibit the proliferation, block the cell cycle, and induce the apoptosis of THP-1 cells, which may be related to inhibition of the PI3K/AKT/mTOR signaling pathway.
探讨虎杖苷对急性单核细胞白血病细胞系THP-1增殖和凋亡的影响及其可能机制。
将THP-1细胞用不同梯度浓度的虎杖苷处理24小时和48小时后，采用CCK-8法检测细胞增殖情况，并计算半数抑制浓度（IC50）。将对数生长期的THP-1细胞分为两组，虎杖苷处理组（用虎杖苷IC50处理）和空白对照组（不用虎杖苷溶液处理），孵育48小时。采用流式细胞术检测细胞凋亡和细胞周期。采用蛋白质印迹法检测PI3K、AKT、p-AKT、mTOR、p-mTOR、p70 S6K和p-p70 S6K蛋白的表达水平。
经虎杖苷处理后，THP-1细胞的增殖受到明显抑制，48小时的IC50为1 800 μmol/L。用1 800 μmol/L虎杖苷溶液处理48小时后，THP-1细胞的凋亡率与空白对照组相比显著升高（<0.05）。细胞周期阻滞在G/G和S期，与空白对照组相比，G/G期细胞比例显著增加，S期细胞比例显著降低（<0.05）。与空白对照组相比，PI3K、AKT、p-AKT、mTOR、p-mTOR、p70 S6K和p-p70 S6K蛋白的表达水平显著降低（<0.05）。
虎杖苷可有效抑制THP-1细胞的增殖，阻滞细胞周期并诱导其凋亡，其机制可能与抑制PI3K/AKT/mTOR信号通路有关。
