基于PI3K/AKT通路研究升降通癃方对前列腺增生细胞的影响

目的:研究升降通癃方通过调节磷脂酰肌醇3-激酶(PI3K)/丝氧酸-苏氨酸蛋白激酶(AKT)信号通路对前列腺增生细胞增殖和凋亡的影响。方法:培养人前列腺增生细胞(BPH-1),随机分为对照组、升降通癃方低、中、高浓度组、阳性组五组，分别给予各组需要的药物处理24 h后，通过四唑盐比色法(CCK8法)检测药物对BPH-1细胞增殖的影响；用细胞划痕实验测定BPH-1的水平迁移能力；通过流式细胞术(FCM)检测升降通癃方对BPH-1细胞细胞凋亡的影响；通过蛋白质印迹法(Western blot)检测药物对细胞中半胱氨酸天冬氨酸蛋白酶3(Caspase-3)、Bcl-2关联X蛋白(Bax)、B淋巴细胞瘤-2(Bcl-2)、磷脂酰肌醇3-激酶(PI3K)、丝氧酸-苏氨酸蛋白激酶(AKT)、重组人α晶状体球蛋白B(Cryab)蛋白表达的影响。结果:加入升降通癃方后，BPH-1的迁移能力明显受到抑制，升降通癃方高、中、低浓度组比较差异有统计学意义(均P<0.05);FCM检测结果显示，升降通癃方组低、中、高浓度组的细胞凋亡率明显高于对照组，差异具有统计学意义(均P<0.05)。Weste...

The effect of Shengjiang Tonglong decoction on prostatic hyperplasia cells based on PI3K/AKT pathway

Objective:To investigate the effect of Shengjiang Tonglong decoction on proliferation and apoptosis by regulating PI3K/AKT signaling pathway.Methods:Human prostatic hyperplasia cells were taken for cell culture,it was randomly divided into 5 groups:control group,low concentration group,medium concentration group,high concentration group,and positive group,After administering the corresponding drugs for 24 h,the effect of drugs on cell proliferation was determined by tetrazole salt colorimetric method.The effect of Shengjiang Tonglong decoction on apoptosis in human prostatic hyperplasia cells was detected by flow cytometry and the effect of protein blotting on the protein expression of Caspase-3,Bax,Bcl-2,PI3K,AKT,and Cryab in cells.The results showed that the migration ability of BPH-1 was significantly reduced in the high,medium and lower concentrations(all P<0.05).Results:FCM showed that the apoptosis rate was significantly higher than that in the blank group(all P<0.05),and the difference was statistical significant.Western blot assay showed that after 24 h of Shengjiang Tonglong decoction treatment,Caspase-3 and Bax were highly expressed in BPH-1 cells,Bcl-2,PI3K,AKT,and Cryab in BPH-1 cells and increased apoptosis rate.Conclusion:It can partly inhibit prostatic hyperplasia cell proliferation,migration and promote its apoptosis by negatively regulating PI3K/AKT signaling pathway by reducing Cryab protein expression.