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黄芪建中汤对感染幽门螺杆菌的GES-1细胞增殖和凋亡影响的药理及分子分析 (原文中“. ”处信息缺失,推测补充为“幽门螺杆菌”使句子完整,具体应根据实际情况确定)

Pharmacological and molecular analysis of the effects of Huangqi Jianzhong decoction on proliferation and apoptosis in GES-1 cells infected with .

作者信息

Hu Jingnan, He Tao, Liu Jianfang, Jia Sujie, Li Bolin, Xu Weichao, Liao Man, Guo Lifang

机构信息

Hebei Province Hospital of Chinese Medicine, Shijiazhuang, China.

Hebei Industrial Technology Institute for Traditional Chinese Medicine Preparation, Shijiazhuang, China.

出版信息

Front Pharmacol. 2022 Sep 29;13:1009705. doi: 10.3389/fphar.2022.1009705. eCollection 2022.

DOI:10.3389/fphar.2022.1009705
PMID:36249768
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9556892/
Abstract

Infection with () can cause chronic gastritis and other digestive tract diseases, and represents a public health concern. Current anti- treatment can result in antibiotic resistance and other adverse reactions. Huangqi Jianzhong decoction (HQJZD) is a prescription form of traditional Chinese medicine for chronic gastritis that increases probiotics and inhibits . In this study, its anti-bacterial activity against receives a preliminary evaluation, and a pharmacology analysis is performed to predict its underlying mechanisms. Human GES-1 cells are divided into a blank control group, a model group, a HQJZD low-dose (2.08 mg·mL), a high-dose group (4.16 mg·mL), and a positive control group (amoxicillin, 5 μg·mL). After culture, the CCK-8 method is used to detect cell viability; flow cytometry is used to detect cell apoptosis rate; and RT-qPCR is used to detect the expression of mRNA virulence factors, including HpPrtC, OPiA, IceA1, and BabA2. Network pharmacology analysis and molecular docking were performed to explore the mechanisms of HQJZD in treating gastritis, based on its anti- infection effect. We noted lower cell survival rates in the model group, but higher apoptosis rates and mRNA expressions of HpPrtC, OPiA, IceA1, and BabA2 than in the control group ( < 0.05). Compared to the model group, the cell survival rate of each dosage group of Huangqi Jianzhong decoction and the positive control group increased significantly, while the apoptosis rate and the mRNA expressions of HpPrtC, OPiA, IceA1, and BabA2 were decreased significantly. The effect in each HQJZD group was dose-dependent ( < 0.05). Network pharmacological analysis involving 159 signaling pathways was used to screen 6 key active components of HQJZD and 102 potential target proteins for the treatment of -related gastritis. The molecular docking results revealed that the 6 active compounds had a strong binding ability with the target proteins of ALB, IL-6, AKT1, IL-1B, and JUN. HQJZD effectively increases the proliferation rate of human GES-1 cells after infection, while reducing the level of apoptosis. The mechanism may be related to multiple components, multiple targets and pathways, which provides a scientific basis for further elucidating the mechanism of action, the pharmacodynamic material basis, and the clinical application of HQJZD against infection.

摘要

感染(幽门螺杆菌)可导致慢性胃炎和其他消化道疾病,是一个公共卫生问题。目前的抗幽门螺杆菌治疗可能会导致抗生素耐药性和其他不良反应。黄芪建中汤(HQJZD)是一种用于治疗慢性胃炎的中药方剂,可增加益生菌并抑制幽门螺杆菌。在本研究中,对其抗幽门螺杆菌活性进行了初步评估,并进行了药理学分析以预测其潜在机制。将人GES-1细胞分为空白对照组、模型组、HQJZD低剂量组(2.08mg·mL)、高剂量组(4.16mg·mL)和阳性对照组(阿莫西林,5μg·mL)。培养后,采用CCK-8法检测细胞活力;采用流式细胞术检测细胞凋亡率;采用RT-qPCR检测mRNA毒力因子(包括HpPrtC、OPiA、IceA1和BabA2)的表达。基于HQJZD的抗感染作用,进行了网络药理学分析和分子对接,以探讨其治疗幽门螺杆菌胃炎的机制。我们注意到模型组的细胞存活率较低,但与对照组相比,HpPrtC、OPiA、IceA1和BabA2的凋亡率和mRNA表达较高(P<0.05)。与模型组相比,黄芪建中汤各剂量组和阳性对照组的细胞存活率显著提高,而凋亡率以及HpPrtC、OPiA、IceA1和BabA2的mRNA表达显著降低。各HQJZD组的效果呈剂量依赖性(P<0.05)。通过涉及159条信号通路的网络药理学分析,筛选出HQJZD的6种关键活性成分和102种治疗幽门螺杆菌相关胃炎的潜在靶蛋白。分子对接结果显示,这6种活性化合物与ALB、IL-6、AKT1、IL-1B和JUN的靶蛋白具有很强的结合能力。HQJZD可有效提高感染后人GES-1细胞的增殖率,同时降低凋亡水平。其机制可能与多种成分、多个靶点和多条途径有关,为进一步阐明HQJZD抗幽门螺杆菌感染的作用机制、药效物质基础及临床应用提供了科学依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1ce/9556892/39a1ac63f096/fphar-13-1009705-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1ce/9556892/39a1ac63f096/fphar-13-1009705-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1ce/9556892/92e88b481606/fphar-13-1009705-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1ce/9556892/c090a4666c70/fphar-13-1009705-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1ce/9556892/31f4e143bb92/fphar-13-1009705-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1ce/9556892/39a1ac63f096/fphar-13-1009705-g006.jpg

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