首页|消癌解毒方抑制H22荷瘤小鼠移植瘤生长及调控Bcl-2/CytC信号通路诱导凋亡实验研究

消癌解毒方抑制H22荷瘤小鼠移植瘤生长及调控Bcl-2/CytC信号通路诱导凋亡实验研究

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目的 探讨消癌解毒方对H22荷瘤小鼠肿瘤生长以及Bel-2/CytC信号通路中关键蛋白表达的影响.方法 构建H22肝癌移植瘤模型,将C57BL/6J小鼠随机分为模型组(生理盐水灌胃)、消癌解毒方低剂量组(10 g·kg-1·d-1灌胃)、消癌解毒方中剂量组(20 g·kg-1·d-1灌胃)、消癌解毒方高剂量组(40 g·kg-1·d-1灌胃)及顺铂组(1 mg·kg-1·d-1腹腔注射),另设空白组(生理盐水灌胃),每组10只.给药11 d,记录各组瘤重,计算抑瘤率,苏木素-伊红(HE)染色观察病理变化,TUNEL试剂盒检测凋亡率,实时荧光定量PCR(Real-time PCR)检测瘤体组织中JAK2、STAT3 mRNA 表达情况,蛋白免疫印迹(Western blot)检测瘤体组织 Bax、Bcl-2、CytC、Caspase-3、Cleaved Caspase-3蛋白表达情况.结果 消癌解毒方高、中、低剂量组及顺铂组均能有效抑制H22荷瘤小鼠瘤体生长,抑瘤率分别为59.9%、34.5%、21.5%、67.1%;病理学改变与模型组相比,给药组病理性核分裂像减少,瘤细胞排列稀疏,表现出较好的抑制作用;TUNEL凋亡检测结果示,消癌解毒方处理后瘤体细胞呈典型凋亡征象,以高剂量组最为显著;Rt-PCR检测发现消癌解毒方干预后各组的JAK2、STAT3 mRNA表达水平下调;Western blot检测发现消癌解毒方对H22荷瘤小鼠干预后,可下调Bel-2蛋白表达,上调Bax、CytC、Cleaved Caspase-3蛋白表达,最终激活Caspase-3蛋白,诱导肿瘤细胞凋亡.结论 消癌解毒方可抑制H22荷瘤小鼠生长及诱导肝癌细胞凋亡,这可能与调控Bel-2/CytC信号通路中关键蛋白表达相关,从而发挥抗肿瘤作用.
Xiao'ai Jiedu Prescription(消癌解毒方)Inhibits Growth of H22 Tumor-Bearing Mice and Regulates Bcl-2/CytC Signaling Pathway to Induce Apoptosis
Objective To investigate the effects of Xiao'ai Jiedu Prescription(消癌解毒方)on tumor growth and the expres-sions of key proteins in Bel-2/CytC signaling pathway in H22 tumor-bearing mice.Methods The H22 hepatocellular carcinoma transplantation tumor model was constructed.C57BL/6J mice were randomly divided into model group(normal saline by gavage),Xiao'ai Jiedu Prescription low-dose group(10 g·kg-1·d-1 gavage),Xiao'ai Jiedu Prescription medium-dose group(20 g·kg-1·d-1gavage),Xiao'ai Jiedu Prescription high-dose group(40 g·kg-1·d-1 gavage),cisplatin group(1 mg·kg-1·d-1,intraperitoneal injection)and blank group(normal saline by gavage),10 mice in each group.After 11 days of administration,the tumor weight was recorded and the tumor inhibition rate was calculated.Pathological changes were observed by Hematoxylin-eosin(HE)staining,the apoptosis rate was detected by TUNEL kit,and the expressions of JAK2 and STAT3 mRNA in tumor tissues were detected by Real-time PCR.The protein expressions of Bax,Bel-2,CytC,Caspase-3 and Cleaved Caspase-3 in tumor tissues were detected by Western blot.Results Xiao'ai Jiedu Prescription high,medium and low dose groups and cisplatin group could inhibit tumor growth in H22 tumor-bearing mice with the inhibitory rates of 59.9%,34.5%,21.5%and 67.1%,respectively.Compared with those in the model group,the pathological mitotic figures were reduced and tumor cells were sparsely arranged in the drug groups,showing a better inhibitory effect.The results of TUNEL showed that the tumor cells showed typical apoptotic signs after Xiao'ai Jiedu Prescription treatment,especially in the high-dose group.Rt-PCR showed that JAK2 and STAT3 mRNA expressions were down-regulated in each dose group of Xiao'ai Jiedu Prescription.Western blot as-say showed that Xiao'ai Jiedu Prescription could up-regulate the expressions of Bax,CytC,Cleaved Caspase-3 protein and down-regulate the expression of Bcl-2 protein in H22 tumor-bearing mice,and finally activate Caspase-3 protein to induce apoptosis of tumor cells.Conclusion Xiao'ai Jiedu Prescription can inhibit the growth of H22 tumor-bearing mice and induce the apoptosis of H22 cells,which may be related to the regulation of the expressions of key proteins in the Bcl-2/CytC signaling pathway,so as to play an anti-tumor role.

Xiao'ai Jiedu Prescription(消癌解毒方)liver cancerBcl-2/CytC signaling pathwayapoptosis

卢曼、李文婷、吴勉华、张羽、费凡、葛慧琳

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南京中医药大学,江苏南京 210023

江苏省中医药防治肿瘤协同创新中心,江苏南京 210023

消癌解毒方 肝癌 Bel-2/CytC信号通路 凋亡

2025

辽宁中医杂志
辽宁中医药大学,辽宁省中医药学会

辽宁中医杂志

北大核心
影响因子:0.815
ISSN:1000-1719
年,卷(期):2025.52(1)