基于转录组测序技术分析三七、黄芪及其配伍对慢性萎缩性胃炎大鼠胃黏膜的作用机制  

Mechanism of Astragalus membranaceus and Panax notoginseng and their compatibility on the gastric mucosa of rats with chronic atrophic gastritis based on RNA-seq technique

作　　者：沈家林 易璐莹[2] 刘力 杜晓泉 曹若彤 郗春华 赵唯含 SHEN Jialin;YI Luying;LIU Li;DU Xiaoquan;CAO Ruotong;XI Chunhua;ZHAO Weihan(Shaanxi University of Chinese Medicine,Xianyang 712046,Shaanxi,China;Changping District Hospital of Integrated Traditional and Western Medicine,Beijing 102208,China;Affiliated Hospital of Shaanxi University of Chinese Medicine,Xianyang 712000,Shaanxi,China)

机构地区：[1]陕西中医药大学,陕西咸阳712046 [2]北京市昌平区中西医结合医院,北京102208 [3]陕西中医药大学附属医院,陕西咸阳712000

出　　处：《现代中西医结合杂志》2024年第23期3219-3229,3238,共12页Modern Journal of Integrated Traditional Chinese and Western Medicine

基　　金：国家自然科学基金资助项目(81804082);陕西省自然科学基金资助项目(2023-JC-YB-667);陕西省中医药管理局科研项目(SZY-KJCYC-2023-019)。

摘　　要：目的基于转录组测序(RNA-Seq)技术探讨三七、黄芪及其配伍对慢性萎缩性胃炎(CAG)大鼠胃黏膜的干预机制。方法17只雄性Wistar大鼠适应性饲养7 d后,随机取4只作为空白组,剩余大鼠采用1-甲基-3-硝基-1-亚硝基胍(MNNG)复合造模法建立CAG模型。采用随机数字表法将造模成功大鼠分为模型组4只、三七组3只、黄芪组3只、三七+黄芪组3只,然后模型组给予去离子水2 mL/d灌胃,三七组给予三七粉冲剂0.7 g/(kg·d)灌胃,黄芪组给予黄芪浸膏3.5 g/(kg·d)灌胃,三七+黄芪组给予三七粉冲剂0.7 g/(kg·d)和黄芪浸膏3.5 g/(kg·d)灌胃,均1次/d,连续灌胃8周。末次灌胃结束后,HE染色观察胃窦组织病理形态,使用RNA-Seq技术分析各组大鼠胃组织差异表达基因,并对差异表达基因进行Gene Ontology(GO)功能富集分析及Kyoto Encyclopedia of Genes and Genomes(KEGG)通路富集分析。结果模型组大鼠胃组织出现肠上皮化生、异型增生等典型萎缩性胃炎表现;各给药组大鼠萎缩性胃炎表现均较模型组轻,无肠上皮化生及异型增生,其中三七+黄芪组病变最轻,其次为黄芪组。转录组数据显示,空白组与模型组间共鉴别得到差异表达基因181个,涉及的主要生物学途径是糖酵解/糖异生、白细胞跨内皮迁移等;三七组与模型组间共鉴别得到差异表达基因116个,涉及的主要生物学途径是维生素消化吸收、p53信号通路、淀粉和蔗糖代谢等;黄芪组与模型组间共鉴别得到差异表达基因556个,涉及的主要生物学途径是维生素B 6代谢、胃酸分泌、p53信号通路等;三七+黄芪组与模型组间共鉴别得到差异表达基因294个,涉及的主要生物学通路为淀粉和蔗糖代谢、p53信号通路、MAPK信号通路、胃酸分泌、糖酵解/糖异生等。结论三七、黄芪及其配伍通过调节多个基因的表达改善CAG大鼠胃黏膜的病理变化。Objective It is to explore the mechanism of Astragalus membranaceus(AM)and Panax notoginseng(PN)and their compatibility in the intervention of gastric mucosa of rats with chronic atrophic gastritis(CAG)based on RNA-sequencing(RNA-Seq).Methods Seventeen male Wistar rats were selected,in which 4 rats were randomly selected as blank group after adjustable feeding for 7 days,and the remaining rats were used to establish models of CAG by 1-methyl-3-nitro-1-nitrosoguanidine(MNNG)composite modeling method.The successfully modeled rats were divided into model group(n=4),PN group(n=3),AM group(n=3),and PN+AM group(n=3)by random number table method.The model group was given deionized water 2 mL/d by gavage,The PN group was given PN powder 0.7 g/(kg·d)by gavage,The AM group was given AM extractum 3.5 g/(kg·d)by gavage,and the PN+AM was given PN powder 0.7 g/(kg·d)and AM extractum 3.5 g/(kg·d)by gavage,all once daily,continuously treated for 8 weeks.At the end of the last gavage,the histopathological morphology of gastric sinusoidal tissues was observed by HE staining,and the differentially expressed genes in the gastric tissues of rats in each group were analyzed by RNA-Seq,and the differentially expressed genes were analyzed by Gene Ontology(GO)function enrichment analysis and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway enrichment analysis.Results Typical atrophic gastritis manifestations such as intestinal epithelialization and heteroplasia appeared in the gastric tissues of rats in the model group;the manifestations of atrophic gastritis in the rats of all administered groups were lighter than those in the model group,without intestinal epithelialization and heteroplasia,among which the lesions in the PN+AM group were the lightest,followed by those in the AM group.The transcriptome data showed that a total of 181 differentially expressed genes were identified between the model group and blank group,and the main biological pathways involved were glycolysis/gluconeogenesis,leukocyte transendothelial migration,

关 键 词：慢性萎缩性胃炎 转录组测序技术 三七 黄芪 

分 类 号：R-332[医药卫生]