首页|黄芪多糖调节PI3K/AKT/mTOR信号通路对良性前列腺增生大鼠细胞凋亡的影响

黄芪多糖调节PI3K/AKT/mTOR信号通路对良性前列腺增生大鼠细胞凋亡的影响

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目的:探讨黄芪多糖(APS)调节PI3K/AKT/mTOR信号通路对良性前列腺增生(BPH)大鼠细胞凋亡的影响。方法:通过摘除双侧睾丸联合皮下注射丙酸睾酮建立BPH大鼠模型,并将建模成功的大鼠随机分为BPH组、APS低剂量(APS-低)组(100 mg/kg APS)、APS中剂量(APS-中)组(200mg/kg APS)、APS高剂量(APS-高)组(400mg/kg APS)、APS-高+PI3K激活剂-胰岛素生长因子1(IGF-1)组(400 mg/kg APS+5 mg/mL IGF-1),干预结束后,电子天平称量前列腺湿质量,计算前列腺指数;TUNEL染色检测前列腺组织细胞凋亡变化;免疫组化检测凋亡基因Caspase-3表达;Western blotting检测通路相关蛋白及凋亡基因Bel-2、Bax表达。结果:与假手术组比较,BPH组前列腺组织病理损伤严重,前列腺湿质量及指数、p-PI3K/PI3K、p-AKT/AKT、p-mTOR/mTOR、Bcl-2蛋白表达显著增加,凋亡指数、Caspase-3阳性表达、Bax表达显著降低(P<0。05);与BPH组比较,APS-低组、APS-中组、APS-高组病理损伤改善,前列腺湿质量及指数、p-PI3K/PI3K、p-AKT/AKT、p-mTOR/mTOR、Bcl-2蛋白表达显著降低,凋亡指数、Caspase-3阳性表达、Bax表达显著增加,不同剂量APS比较差异有统计学意义(P<0。05);与APS-高组比较,APS-高+IGF-1组病理损伤稍加重,前列腺湿质量及指数、p-PI3K/PI3K、p-AKT/AKT、p-mTOR/mTOR、Bcl-2蛋白表达显著增加,凋亡指数、Caspase-3阳性表达、Bax表达显著降低(P<0。05)。结论:APS可通过抑制PI3K/AKT/mTOR信号通路促进BPH大鼠细胞凋亡,有效抑制BPH进展。
Effect of Astragalus Polysaccharides on Cell Ppoptosis in Rats with Benign Prostatic Hyperplasia by Regulating the PI3K/AKT/mTOR Signaling Pathway
[Absrtact]Objective:To investigate the effect of Astragalus polysaccharides(APS)on cell apoptosis in rats with benign prostatic hyperplasia(BPH)by regulating the PI3K/AKT/mTOR signaling pathway.Methods:A BPH rat model was established by bilateral testicular removal combined with subcutaneous injection of testosterone propionate.The successfully modeled rats were randomly separated into BPH group,APS low dose(APS low)group(100 mg/kg APS),APS medium dose(APS medium)group(200 mg/kg APS),APS high dose(APS high)group(400 mg/kg APS),and APS high dose+PI3K activator insulin growth factor 1(IGF-1)group(400 mg/kg APS+5 mg/mL IGF-1).After the intervention,an electronic balance was used to weigh the wet weight of the prostate,and the prostate index was calculated.TUNEL staining was applied to detect changes in apoptosis of prostate tissue cells.Immunohistochemistry was applied to detect the expression of the apoptotic gene Caspase-3.Western blotting was applied to detect the expression of pathway related proteins and apoptotic genes Bcl-2 and Bax.Results:Compared with the sham surgery group,the BPH group showed severe pathological damage to the prostate tissue.The prostate wet weight and index,p-PI3K/PI3K,p-AKT/AKT,p-mTOR/mTOR,and Bcl-2 protein expression greatly increased in BPH group,while the apoptosis index,Caspase-3 positive expression,and Bax expression greatly reduced in BPH group(P<0.05).Compared with the BPH group,the pathological damage was improved in the APS low group,APS medium group,and APS high group.The prostate wet weight and index,p-PI3K/PI3K,p-AKT/AKT,p-mTOR/mTOR,and Bcl-2 protein expression reduced in APS low group,APS medium group,and APS high group,while the apoptosis index,Cacpase-3 positive expression,and Bax expression increased greatly in APS low group,APS medium group,and APS high group.There was statistical difference among different doses of APS(P<0.05).Compared with the APS high group,the pathological damage was slightly aggravated in APS high+IGF-1 group.The prostate wet weight and index,p-PI3K/PI3K,p-AKT/AKT,p-mTOR/mTOR,and Bcl-2 protein expression increased greatly in APS high+IGF-1 group,while the apoptosis index,Caspase-3 positive expression,and Bax expression reduced greatly in APS high+IGF-1 group(P<0.05).Conclusion:APS can promote cell apoptosis in BPH rats and effectively inhibit the progression of BPH by inhibiting the PI3K/AKT/mTOR signaling pathway.

benign prostatic hyperplasiaPI3K/AKT/mTOR signaling pathwayAstragalus polysaccharidescell apoptosisrat

赵猛、孙一诺、齐爽、郑雪

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黑龙江中医药大学附属第一医院,黑龙江 哈尔滨 150040

黑龙江省中医医院,黑龙江 哈尔滨 150000

哈尔滨京恩肾病医院,黑龙江 哈尔滨 150036

良性前列腺增生 PI3K/AKT/mTOR信号通路 黄芪多糖 细胞凋亡 大鼠

黑龙江省卫生健康委科研课题

20220404051077

2024

中医药导报
湖南省中医药学会 湖南省中医管理局

中医药导报

CSTPCD
影响因子:0.952
ISSN:1672-951X
年,卷(期):2024.30(8)