基于PI3K/Akt信号通路探讨蠲浊调冲汤诱导细胞凋亡治疗子宫内膜息肉的作用机制OA
Investigation of the Mechanism of Action of Juanzhuo Tiaochong Decoction in Treating Endometrial Polyp by Inducing Apoptosis via the PI3K/Akt Signaling Pathway
目的 探讨蠲浊调冲汤(JZTCT)通过PI3K/Akt信号通路诱导细胞凋亡治疗子宫内膜息肉(EP)的作用机制.方法 采用酶消法从EP患者手术标本中分离并培养原代细胞,经免疫荧光法鉴定.40只SD大鼠随机分为空白对照组、JZTCT低剂量组、JZTCT中剂量组、JZTCT高剂量组,每组10只.JZTCT低、中、高剂量组分别按11.7、23.4、46.8 g/(kg·d)灌胃给予相应浓度的JZTCT水煎液,空白对照组灌胃等体积生理盐水,每日2次,连续灌胃7 d.末次灌胃结束后,大鼠禁食不禁水12 h,腹主动脉采血,将分离得到的相应血清分别作用于EP细胞,即空白组(EP原代细胞+10%空白对照组血清),低剂量组(EP原代细胞+10%JZTCT低剂量组含药血清),中剂量组(EP原代细胞+10%JZTCT中剂量组含药血清)和高剂量组(EP原代细胞+10%JZTCT高剂量组含药血清).采用CCK-8法检测各组细胞活力,流式细胞术检测细胞凋亡率,qRT-PCR检测PI3K、Akt mRNA表达,Western blot检测凋亡相关因子及PI3K/Akt通路关键蛋白的表达水平.结果 与空白组比较,JZTCT含药血清可显著抑制EP原代细胞的增殖并诱导其凋亡,显著抑制PI3K、Akt mRNA表达,上调Bax和Caspase-3蛋白表达,下调Bcl-2、p-PI3K/PI3K及p-Akt/Akt表达(P<0.05).结论 蠲浊调冲汤可通过抑制PI3K/Akt信号通路,调控下游凋亡相关因子,从而发挥治疗子宫内膜息肉的作用.
Objective To investigate the mechanism of action of Juanzhuo Tiaochong Decoction(JZTCT)in treating endometrial polyp(EP)through the induction of apoptosis via the PI3K/Akt signaling pathway.Methods Primary cells were isolated and cultured from surgical specimens of EP patients via enzymatic digestion,identified by immunofluorescence.Forty SD rats were randomly divided into four groups:blank control group,low-,medium-,and high-dose JZTCT groups,with 10 rats in each group.Rats in low-,medium-,and high-dose JZTCT groups were gavaged with JZTCT at the corresponding doses of 11.7,23.4,and 46.8 g/(kg·d)respectively,while rats in blank control group were gavaged with an equal volume of physiological saline.All groups were administrated twice daily for 7 consecutive days.After the final gavage,rats were fasted(with free access to water)for 12 h,and blood samples were collected from the abdominal aorta.EP cells were treated with the corresponding serum samples isolated,then the cells were divided into the following groups:blank group(EP primary cells+10%serum from the blank control group),low-dose group(EP primary cells+10%drug-containing serum from the low-dose JZTCT group),medium-dose group(EP primary cells+10%drug-containing serum from the medium-dose JZTCT group),and high-dose group(EP primary cells+10%drug-containing serum from the high-dose JZTCT group).Cell viability was assessed using the CCK-8 assay;Apoptosis rates were measured by flow cytometry;mRNA expression levels of PI3K and Akt were detected by qRT-PCR;Protein expression levels of apoptosis-related factors and key proteins in the PI3K/Akt pathway were evaluated by Western blot.Results Compared with the blank group,JZTCT-containing serum significantly inhibited the proliferation of EP primary cells and induced apoptosis,markedly suppressed the mRNA expression of PI3K and Akt,upregulated the protein expression of Bax and Caspase-3,and downregulated the expression of Bcl-2,p-PI3K/PI3K,and p-Akt/Akt(P<0.05).Conclusion JZTCT can exert its therapeutic effects on EP by inhibiting the PI3K/Akt signaling pathway and regulating downstream apoptosis-related factors.
赵桢;刘芳媛;丁丹妮;韩凤娟
黑龙江中医药大学,黑龙江 哈尔滨 150040黑龙江中医药大学附属第一医院,黑龙江 哈尔滨 150040黑龙江中医药大学附属第一医院,黑龙江 哈尔滨 150040黑龙江中医药大学附属第一医院,黑龙江 哈尔滨 150040
蠲浊调冲汤子宫内膜息肉细胞凋亡PI3K/Akt信号通路
Juanzhuo Tiaochong DecoctionEndometrial polypApoptosisPI3K/Akt signaling pathway
《中医药信息》 2026 (3)
15-20,6
中医药循证能力提升项目(国中医药科技中药便函[2023]24号)黑龙江省中医药科研项目(ZYW2024-014)
评论