Xinjiang Medical University, Urumqi 830017, Xinjiang, China.
Contrast Media Mol Imaging. 2022 Aug 10;2022:3483774. doi: 10.1155/2022/3483774. eCollection 2022.
To analyze and test the effect of and on the network pharmacology of MAPK (mitogen-activated protein kinase) and TNF (tumor necrosis factor) signaling channels and inflammatory factor target gene regulation in successful modeling of chronic atrophic gastritis rats.
Rats with chronic atrophic gastritis that were modeled successfully were randomly divided into control and study groups and were treated with conventional western medicine or Rhizoma phragmitis and Rhizoma curcumae, respectively. The pharmacological mechanism of action and efficacy were evaluated.
The treatment efficiency was 76.32% and 97.37% in the control and study group, respectively. After treatment, the serum tumor necrosis factor- (TNF-) and serum malondialdehyde (MDA) levels in the study group were lower than those in the control group and the serum epidermal growth factor (EGF) and superoxide dismutase (SOD) levels in the study group were higher than those in the control group ( < 0.05); the pain behavioral scores in the study group were lower than those in the control group, and the free acid quantity and total acid quantity in the study group were higher than those in the control group ( < 0.05); the serum MTL index in the study group was higher than that in the control group, and the serum gastrin (GAS) and pepsinogen I (PG I) indices in the study group were lower than those in the control group ( < 0.05); the number of 24-hour reflux in the study group was less than that in the control group ( < 0.05), and the longest reflux time in the study group was lower than that in the control group ( < 0.05).
Based on the network pharmacological results, and will modulate MAPK, TNF signaling circuits, and inflammatory factor target genes in the chronic atrophic gastritis rat model. This treatment protocol is efficient and beneficial to enhance the gastric function of the chronic atrophic gastritis rat model, while it can alleviate the inflammatory response and significantly reduce the number and duration of reflux, which is a safe and reliable treatment modality.
分析和检测 和 对成功建立的慢性萎缩性胃炎大鼠模型中 MAPK（丝裂原活化蛋白激酶）和 TNF（肿瘤坏死因子）信号通路以及炎症因子靶基因调控的网络药理学作用。
成功建立慢性萎缩性胃炎大鼠模型后，将其随机分为对照组和研究组，分别采用常规西药或芦根和莪术进行治疗，评价其药理作用机制和疗效。
对照组和研究组的治疗效率分别为 76.32%和 97.37%。治疗后，研究组血清肿瘤坏死因子-（TNF-）和血清丙二醛（MDA）水平低于对照组，血清表皮生长因子（EGF）和超氧化物歧化酶（SOD）水平高于对照组（均<0.05）；研究组疼痛行为评分低于对照组，游离酸量和总酸量高于对照组（均<0.05）；研究组血清胃动素（MTL）指数高于对照组，血清胃泌素（GAS）和胃蛋白酶原 I（PG I）指数低于对照组（均<0.05）；研究组 24 小时反流次数少于对照组，最长反流时间低于对照组（均<0.05）。
基于网络药理学结果， 和 可调节慢性萎缩性胃炎大鼠模型中 MAPK、TNF 信号通路和炎症因子靶基因。该治疗方案有效且有利于增强慢性萎缩性胃炎大鼠模型的胃功能，同时减轻炎症反应，显著减少反流次数和持续时间，是一种安全可靠的治疗方式。
