吴茱萸碱调控EGFR/MAPK/ERK通路对Hp诱导慢性萎缩性胃炎大鼠的作用机制  

Mechanism of Evodiamine on Gastrointestinal Function in Helicobacter Pylori-induced Chronic Atrophic Gastritis Rats via Regulating EGFR/MAPK/ERK Pathway

作　　者：李莉[1] 杨伟[1] 梁春耕 尚莹莹[1] LI Li;YANG Wei;LIANG Chungeng(Shanghai Jiading District Hospital of Traditional Chinese Medicine,Shanghai 201800,China)

机构地区：[1]上海市嘉定区中医医院,上海201800

出　　处：《河北医学》2025年第2期215-223,共9页Hebei Medicine

基　　金：上海市卫生系统优秀青年医学人才培养项目,(编号:PWRq2022-010)。

摘　　要：目的:探讨吴茱萸碱通过调控EGFR/MAPK/ERK信号通路对Hp诱导的慢性萎缩性胃炎(CAG)大鼠胃肠道功能的影响。方法:选取40只SD雄性大鼠,随机选取10只大鼠将其作为空白组,其余30只建立Hp诱导的CAG模型,成功27只,失败3只,将其随机分为模型组、吴茱萸碱组、吴茱萸碱+抑制剂组,每组各9只大鼠。给予吴茱萸碱组大鼠20mg/kg吴茱萸碱,吴茱萸碱+抑制剂组大鼠20mg/kg吴茱萸碱+0.3g/kg维酶素。空白组和模型组大鼠不做任何处理。比较各组大鼠病理评分、胃黏膜血流量、胃内残留率、胃肠激素指标、炎症因子、血清特异标志物、小肠推进率、EGFR、MAPK、ERK mRNA和蛋白表达。结果:与空白组相比,模型组、吴茱萸碱+抑制剂组萎缩性评分(1.06±0.33)(0.98±0.31)、炎性活动性评分(1.27±0.41)(1.11±0.36)、MTL(239.41±20.74)(237.45±20.85)、IL-12、IL-1β、IL-8、IL-17、CXCL1、胃内残留率(76.95±12.35)(74.35±13.05)升高,GMBF、SS(10.10±4.03)(11.39±4.09)、小肠推进率(52.06±3.42)(53.18±3.73)、GAS(39.24±6.78)(40.25±6.76)、G-17下降(P<0.05);与模型组相比,吴茱萸碱组萎缩性评分(0.19±0.05)、炎性活动性评分(0.23±0.06)、MTL(150.78±13.01)、IL-12、IL-1β、IL-8、IL-17、胃内残留率(54.19±8.52)、CXCL1下降,GMBF、SS(25.96±5.74)、小肠推进率(62.19±5.08)、GAS(65.37±9.49)、G-17上升(P<0.05);与吴茱萸碱组相比,吴茱萸碱+抑制剂组萎缩性评分、炎性活动性评分、胃内残留率、MTL、IL-12、IL-1β、IL-8、IL-17、CXCL1升高,GMBF、SS、GAS、小肠推进率、G-17下降(P<0.05)。与空白组相比,模型组、吴茱萸碱+抑制剂组EGFR(3.66±0.52)(3.64±0.51)、MAPK(2.14±0.15)(2.13±0.15)、ERK(2.21±0.17)(2.19±0.16)mRNA和蛋白表达上升(P<0.05);与模型组相比,吴茱萸碱组EGFR(1.03±0.02)、MAPK(0.68±0.08)、ERK(0.80±0.09)mRNA和蛋白表达下降(P<0.05);与吴茱萸碱组相比,吴茱萸碱+抑制剂组EGFR、MAPK、ERK mRNA和蛋白表达上升(P<0.05)。Objective:To investigate the effect of evodiamine on gastrointestinal function in Helicobacter pylori(Hp)-induced chronic atrophic gastritis(CAG)rats via regulating epidermal growth factor receptor(EGFR)/mitogen-activated protein kinases(MAPK)/extracellular signal-regulated kinases(ERK)signaling pathway.Methods:Forty SD male rats were selected,10 rats were induced blank control,and the remaining 30 were induced to establish a Hp-induced CAG model.Except for three failures,27 success rates were randomly divided into model group(transfection of HB),evodiamine group(20 mg/kg evodiamine),evodiamine+inhibitor group(20 mg/kg evodiamine+0.3 g/kg vitase),and 9 rats in each group.Rats in blank group and model group were not treated.The pathological score,gastric mucosal blood flow,gastric residual rate,gastrointestinal hormone,inflammatory factors,serum-specific markers,propulsion rate of small intestinal,EGFR,MAPK,ERK mRNA and protein expression were compared in each group.Results:Compared to the blank group,atrophy score(1.06±0.33)(0.98±0.31),inflammatory activity score(1.27±0.41)(1.11±0.36),motilin(MTL)(239.41±20.74)(237.45±20.85),interleukin(IL)-12,IL-1β,IL-8,IL-17,C-X-C motif ligand 1(CXCL1),and intragastric retention(76.95±12.35)(74.35±13.05)in the model group and the evodiamine+inhibitor group were significantly elevated,gastric mucosal blood flow(GMBF),somatostatin(SS)(10.10±4.03)(11.39±4.09),propulsion rate of small intestinal(52.06±3.42)(53.18±3.73),gastrin(GAS)(39.24±6.78)(40.25±6.76),and gastrin-17(G-17)were significantly decreased(P<0.05).Compared with the model group,atrophy score(0.19±0.05),inflammatory activity score(0.23±0.06),MTL(150.78±13.01),IL-12,IL-1β,IL-8,IL-17,intragastric retention rate(54.19±8.52),and CXCL1 were significantly decreased in the evodiamine group,but GMBF,SS(25.96±5.74),propulsion rate of small intestinal(62.19±5.08),GAS(65.37±9.49),and G-17 were significantly increased(P<0.05).Atrophic score,inflammatory activity score,intragastric retention rate,MTL,IL-12,IL-

关 键 词：吴茱萸碱 表皮生长因子受体 丝裂原激活蛋白激酶 细胞外信号调节激酶 幽门螺杆菌 慢性萎缩性胃炎 

分 类 号：R285.5[医药卫生—中药学]