Yang Zi-Yan, Li Zi-Lin, Zhang Cui-Xiang, Huang Li-Jin, Wang Han, Li Xue-Ying, Chen Gui-Yuan
College of Basic Medicine, Dali University Dali 671000, China.
College of Basic Medicine, Dali University Dali 671000, China Yunnan Provincial Key Laboratory of Entomology Biopharmaceutical R&D Dali 671000, China.
Zhongguo Zhong Yao Za Zhi. 2024 Oct;49(19):5307-5314. doi: 10.19540/j.cnki.cjcmm.20240611.702.
Based on the signaling pathway of phosphoinositide 3-kinase(PI3K)/protein kinase B(Akt)/mammalian target of rapamycin(mTOR), pathway-related phosphatase and tensin homolog(PTEN), B-cell lymphoma-2(Bcl-2), and Bcl-2-associated X protein(BAX), the mechanism of Rose roxburghii polysaccharides in inhibiting proliferation and inducing apoptosis of prostate cancer DU145 cells was explored, as well as the antioxidant activity of R. roxburghii polysaccharides. Prostate cancer DU145 cells were treated with different concentrations of R. roxburghii polysaccharides. The effect of R. roxburghii polysaccharides on the proliferation of DU145 cells was detected by the CCK-8 method, and the effect of R. roxburghii polysaccharides on the migration of DU145 cells was detected by cell scratch test. In addition, a Transwell assay was conducted to detect the effect of R. roxburghii polysaccharides on the invasion ability of DU145 cells. The apoptosis of DU145 cells induced by R. roxburghii polysaccharides was detected by flow cytometry. Real-time PCR and Western blot were used to detect the effects of R. roxburghii polysaccharides on the mRNA and protein expression levels of PI3K, Akt, mTOR, PTEN, BAX, and Bcl-2 in DU145 cells. DPPH and ABTS assays were used to determine the antioxidant activity of R. roxburghii polysaccharides in vitro. The results showed that R. roxburghii polysaccharides inhibited the prolife-ration, migration, and invasion of DU145 cells. Flow cytometry analysis showed that compared with that of the control group, the apoptosis rate of DU145 cells in groups treated with R. roxburghii polysaccharides was increased with the increase in the concentration of R. roxburghii polysaccharides, and its inhibition was positively correlated with the concentration of R. roxburghii polysaccharides. R. roxburghii polysaccharides inhibited the PI3K/Akt/mTOR pathway and induced apoptosis of DU145 cells by up-regulating the protein and gene expression of PTEN and BAX and down-regulating the expression of Akt, PI3K, mTOR, and Bcl-2. R. roxburghii polysaccharides could scavenge ABTS and DPPH radicals to a certain extent, suggesting that R. roxburghii polysaccharides may induce the apoptosis of DU145 cells by scavenging intracellular ROS. R. roxburghii polysaccharides may inhibit the proliferation of DU145 cells and induce its apoptosis by inhibiting the PI3K/Akt/mTOR pathway and clearing intracellular ROS.
基于磷酸肌醇3激酶（PI3K）/蛋白激酶B（Akt）/雷帕霉素哺乳动物靶蛋白（mTOR）信号通路、通路相关的磷酸酶和张力蛋白同源物（PTEN）、B细胞淋巴瘤-2（Bcl-2）以及Bcl-2相关X蛋白（BAX），探讨了刺梨多糖抑制前列腺癌DU145细胞增殖和诱导其凋亡的机制，以及刺梨多糖的抗氧化活性。用不同浓度的刺梨多糖处理前列腺癌DU145细胞。采用CCK-8法检测刺梨多糖对DU145细胞增殖的影响，采用细胞划痕试验检测刺梨多糖对DU145细胞迁移的影响。此外，进行Transwell实验检测刺梨多糖对DU145细胞侵袭能力的影响。采用流式细胞术检测刺梨多糖诱导DU145细胞凋亡的情况。采用实时荧光定量PCR和蛋白质免疫印迹法检测刺梨多糖对DU145细胞中PI3K、Akt、mTOR、PTEN、BAX和Bcl-2的mRNA和蛋白表达水平的影响。采用DPPH和ABTS法测定刺梨多糖的体外抗氧化活性。结果表明，刺梨多糖抑制DU145细胞的增殖、迁移和侵袭。流式细胞术分析显示，与对照组相比，刺梨多糖处理组DU145细胞的凋亡率随刺梨多糖浓度的增加而升高，其抑制作用与刺梨多糖浓度呈正相关。刺梨多糖通过上调PTEN和BAX的蛋白及基因表达，下调Akt、PI3K、mTOR和Bcl-2的表达，抑制PI3K/Akt/mTOR通路并诱导DU145细胞凋亡。刺梨多糖能在一定程度上清除ABTS和DPPH自由基，提示刺梨多糖可能通过清除细胞内活性氧诱导DU145细胞凋亡。刺梨多糖可能通过抑制PI3K/Akt/mTOR通路和清除细胞内活性氧来抑制DU145细胞的增殖并诱导其凋亡。
