Mechanism of Evodiamine on Gastrointestinal Function in Helicobacter Pylori -induced Chronic Atrophic Gastritis Rats via Regulating EGFR/MAPK/ERK Pathway
LI Li, YANG Wei, LIANG Chungeng, et al
Shanghai Jiading District Hospital of Traditional Chinese Medicine, Shanghai 201800, China
Abstract：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-1β, IL-8, IL-17, and CXCL1 were significantly elevated, and GMBF, SS, GAS, propulsion rate of small intestinal, and G-17 were significantly decreased in the evodiamine +inhibitor group compared with the evodiamine group (P < 0.05). EGFR (3.66±0.52) (3.64±0.51), MAPK (2.14±0.15) (2.13±0.15), and ERK (2.21±0.17) (2.19±0.16) mRNA and protein expression were increased in the model group and evodiamine +inhibitor group compared with the blank group (P<0.05). EGFR (1.03±0.02), MAPK (0.68±0.08), and ERK (0.80±0.09) mRNA and protein expression were decreased in the evodiamine group compared with the model group (P<0.05). EGFR, MAPK, and ERK mRNA and protein expression were elevated in the evodiamine +inhibitor group compared with the evodiamine group (P < 0.05). Conclusion: Evodiamine can effectively improve the inflammatory response in Hp-induced CAG rats, improve the secretion of gastrointestinal hormones via regulating EGFR/MAPK/ERK signaling pathway.
李莉, 杨伟, 梁春耕, 尚莹莹. 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[J]. 河北医学, 2025, 31(2): 215-223.
LI Li, YANG Wei, LIANG Chungeng, et al. Mechanism of Evodiamine on Gastrointestinal Function in Helicobacter Pylori -induced Chronic Atrophic Gastritis Rats via Regulating EGFR/MAPK/ERK Pathway. HeBei Med, 2025, 31(2): 215-223.
[1] Shah S C,Piazuelo M B,Kuipers E J,et al.AGA cinical practice update on the diagnosisand management of atrophic gastritis:expert review[J].Gastroenterology,2021,161(4):1325-1332. [2] 李有连,张秉丽,霍成英,等.吴茱萸碱对酒精性胃溃疡大鼠胃黏膜上皮细胞的保护作用[J].中南医学科学杂志,2022,50(2):184-189. [3] Cao T,Lu Y,Wang Q,et al.ACGA/EGFR/GATA 2positive feed back circuitc on fersche moresis tanceing astric cancer[J].Clin Invest,2022,132(6):154074. [4] 刘远婷,李慧,丁甜甜,等.加味沙参麦冬汤调节EGFR/MAPK信号通路对慢性萎缩性胃炎大鼠的保护作用研究[J].吉林中医药,2022,42(7):812-816. [5] 惠桃,柏江锋,杭亮.基于Hippo/TAZ信号通路探讨胃苏颗粒对幽门螺杆菌诱导的慢性萎缩性胃炎的作用[J].内蒙古医科大学学报,2023,45(3):292-296. [6] Zhang Y,Yang Q,Song B,et al.Efficacy and safety of piwei peiyuan prescription in the treatment of chronic trophic gastritis:am ulticenter,double-blind,double-simulated,randomized,controlled clinical trial[J].Medicine (Baltimore),2024,103(19):37981. [7] 周志鹏,韦维,陈丽,等.安胃汤对CAG大鼠 NLRP3/Caspase-1/IL-1β信号轴细胞焦亡调控研究[J].时珍国医国药,2022,33(12):2885-2888. [8] 白雪峰,谭娟,高枫.理中汤对慢性萎缩性胃炎模型大鼠胃黏膜保护作用及对ADAM17、EGFR蛋白的影响[J].中医药导报,2021,27(10):32-36. [9] Yang J Y,Woo H J,Lee P,et al.Induction of apoptosis and effect on the FAK/AKT/mTOR signal path way by evodia mine in gastric cancer cells[J].Curr Issues Mol Biol,2022,44(9):4339-4349. [10] Rashd M,Shah1 S G,Verma T,et al.Tumor-specific over expression of his tonegene,H3C14 in gastri c can ceris mediated through EGFR-FOXC1 axis[J].Biochim Biophys Acta Gene Regul Mech,2021,1864(4-5):194703.
2025, Vol. 31 
冀公网安备13080202000786号