机构地区:[1]宁波市医疗中心李惠利医院,浙江宁波315000 [2]广西中医药大学基础医学院,广西南宁530200
出 处:《中华中医药学刊》2022年第4期246-250,共5页Chinese Archives of Traditional Chinese Medicine
基 金:浙江省中医药科技计划(20202b228)。
摘 要:目的探究经方蠲痛饮对子宫内膜异位症(endometriosis,EMS)大鼠的作用及其作用机制。方法采用自体子宫内膜移植法建立EMS大鼠模型。将大鼠随机分为对照组、造模组、Cediranib(AZD2171)药物组、DMSO组以及高、中、低剂量蠲痛饮造模组。对照组、造模组每天给予生理盐水1 mL/100 g灌胃。高、中、低剂量蠲痛饮造模组每天分别给予高、中、低剂量(42.9、14.3、4.8 g/kg)蠲痛饮灌胃。Cediranib(AZD2171)药物组、DMSO组分别给予Cediranib、DMSO(4 mg/kg)腹腔注射。各组连续用药14 d。应用酶联免疫吸附法、蛋白免疫印迹法及实时荧光定量PCR等分子生物学技术检测大鼠血清中肿瘤坏死因子-α(tumor necrosis factorα,TNF-α)、血管内皮生长因子(vascular endothelial growth factor,VEGF)、白细胞介素-6(Interleukin 6,IL-6)及子宫内膜组织中PI3K、Akt、mTOR的表达。结果使用不同剂量蠲痛饮后,大鼠异位灶体积均小于造模组,差异具有统计学意义(P<0.05);TNF-α、IL-6、VEGF的表达均低于造模组,差异具有统计学意义(P<0.05)。造模组的大鼠子宫组织中PI3K、Akt、mTOR的表达均明显高于对照组,Cediranib(AZD2171)药物组的大鼠子宫组织中PI3K、Akt、mTOR的表达均明显低于DMSO组,差异均具有统计学意义(P<0.05)。结论子宫内膜异位症发生发展过程中会过度激活血管内皮生长因子表达,激活PI3K/Akt/mTOR经典信号通路;经方蠲痛饮可以通过降低大鼠炎症因子TNF-α、IL-6及血管内皮生长因子表达水平,抑制异位组织的血管生成,抑制异位子宫内膜生成,达到治疗子宫内膜异位症的目的。Objective To explore the effect of Juantongyin on endometriosis(EMS)rats and its mechanism.Methods The EMS Rat model was established by autologous endometrial transplantation.The rats were randomly divided into control group,model group,Cediranib(AZD2171)group,DMSO group,high-dose Juantongyin model group,medium-dose Juantongyin model group,and low-dose Juantongyin model group.Control group and model group were given saline(1 mL/100 g)by gavage every day.The high-dose,medium-dose and low-dose Juantongyin model groups were respectively given high,medium-dose and low-dose Juantongyin(42.9 g,14.3 g,4.8 g/kg,respectively)by gavage.Cediranib(AZD2171)group and DMSO group were respectivelygiven Cediranib and DMSO(4 mg/kg)by intraperitoneal injection.The administration lasted for 14 days.ELISA,Western blot and Real-time PCR were used to detect the levels of expression of tumor necrosis factor-α(TNF-α),vascular endothelial growth factor(VEGF)and interleukin-6(IL-6)in rat serum,and PI3K,Akt and mTOR in endometrial tissue.Results:After treatment with different doses of Juantongyin,the volume of ectopic tissue in those rats was smaller than that in model group,and the difference was statistically significant(P<0.05).The levels of expression of TNF-α,IL-6,VEGF were lower than those in model group,and the differences were statistically significant(P<0.05).The levels of expression of PI3K,Akt and mTOR in uterine tissues of rats in the model group were significantly higher than those in the control group,and those were significantly lower in Cediranib(AZD2171)group than those in the DMSO group(P<0.05).Conclusions During the development and progression of endometriosis,vascular endothelial growth factor expression is activated ex-cessively and the classic PI3K/Akt/mTOR signaling pathway is activated.By reducing the expression levels of inflammatory factors,such as TNF-αand IL-6,and vascular endothelial growth factor in rats,Juantongyin can inhibit the angiogenesis of ectopic tissues and the formation of ectopic endometriosis,t
关 键 词:经方蠲痛饮 血管内皮生长因子 PI3K 子宫内膜异位症
分 类 号:R271.911.71[医药卫生—中西医结合]
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