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Improvement effects of glycyrrhizin on
Helicobacter pylori -associated gastritis in rats and its mechanism- ZHONGGUO YAOFANG Vol. 35, Issue 2, Pages: 166-171(2024)
- 作者机构：
1.贵州中医药大学第一临床医学院，贵阳 550001
2.贵州医科大学临床微生物与免疫学教研室，贵阳 550001
3.中国中医科学院广安门医院传染病科，北京 100053
4.贵州中医药大学第一附属医院脾胃病科，贵阳 550001
- 作者简介：
- 基金信息：
DOI：10.6039/j.issn.1001-0408.2024.02.08
CLC： R965;R285.5Published：30 January 2024，
Received：10 May 2023，
Revised：27 December 2023，
扫 描 看 全 文
刘誉华,刘莲,汪九重等.甘草甜素对大鼠幽门螺杆菌相关性胃炎的改善作用及机制 Δ[J].中国药房,2024,35(02):166-171.
LIU Yuhua,LIU Lian,WANG Jiuchong,et al.Improvement effects of glycyrrhizin on Helicobacter pylori-associated gastritis in rats and its mechanism[J].ZHONGGUO YAOFANG,2024,35(02):166-171.
刘誉华,刘莲,汪九重等.甘草甜素对大鼠幽门螺杆菌相关性胃炎的改善作用及机制 Δ[J].中国药房,2024,35(02):166-171. DOI： 10.6039/j.issn.1001-0408.2024.02.08.
LIU Yuhua,LIU Lian,WANG Jiuchong,et al.Improvement effects of glycyrrhizin on Helicobacter pylori-associated gastritis in rats and its mechanism[J].ZHONGGUO YAOFANG,2024,35(02):166-171. DOI： 10.6039/j.issn.1001-0408.2024.02.08.
摘要
目的
2
探讨甘草甜素（GL）对大鼠幽门螺杆菌（HP）相关性胃炎的改善作用及机制。
方法
2
以接种1×10
9
cfu/mL HP建立HP相关性胃炎大鼠模型，将造模成功大鼠随机分为模型组、阳性对照组（HP标准四联方案）和GL低、中、高剂量组（5、20、50 mg/kg），每组12只；另取12只正常大鼠作为正常对照组。除正常对照组和模型组大鼠灌胃等体积生理盐水外，其他各组大鼠灌胃相应药物，每天1次，连续30 d。给药结束后大鼠行
13
C尿素呼气试验，记录超基准值（DOB）；观察大鼠胃黏膜组织病理变化和细胞形态学变化，并进行病理评分；检测大鼠胃黏膜组织中白细胞介素8（IL-8）、IL-1β、肿瘤坏死因子α（TNF-α）、活性氧（ROS）、丙二醛（MDA）水平，高迁移率族蛋白B1（HMGB1）、核因子κB（NF-κB）mRNA相对表达量，一氧化氮合酶（iNOS）、HMGB1蛋白相对表达量以及NF-κB p65磷酸化水平。
结果
2
与正常对照组比较，模型组大鼠DOB值，胃黏膜组织病理评分，IL-8、IL-1β、TNF-α、ROS、MDA水平，HMGB1、NF-κB mRNA相对表达量，iNOS、HMGB1蛋白相对表达量和NF-κB p65磷酸化水平均显著升高（
P
＜0.05）；大鼠胃黏膜上皮细胞结构不完整且数量减少，细胞碎片及空泡增多，细胞固缩明显。与模型组比较，GL各剂量组和阳性对照组上述指标变化均显著逆转（
P
＜0.05），且GL高剂量组上述指标变化均较GL低、中剂量组更显著（
P
＜0.05）；大鼠胃黏膜细胞病理变化均改善。
结论
2
GL可能通过抑制HMGB1/NF-κB信号通路的激活，抑制炎症和氧化应激反应，从而减轻HP引起的胃黏膜损伤。
Abstract
OBJECTIVE
2
To investigate the improvement effects of glycyrrhizin （GL） on
Helicobacter pylori
（HP）-associated gastritis in rats and its mechanism.
METHODS
2
HP-associated gastritis rat model was induced by inoculating with 1×10
9
cfu/mL HP. The model rats were randomly divided into model group， positive control group （HP standard quadruple group）， GL low-dose， medium-dose and high-dose groups （5， 20， 50 mg/kg）， with 12 rats in each group. Another 12 healthy rats were selected as normal control group. Except the normal control group and model group were given constant volume of normal saline intragastrically， the other groups were given corresponding drugs intragastrically， once a day， for 30 consecutive days. After administration， rats received
13
C urea breath test， and delta-over-baseline （DOB） was recorded； the pathological and cellular morphological changes of gastric mucosa in rats were observed， and pathological scoring was performed； the levels of interleukin-8 （IL-8）， IL-1β， tumor necrosis factor-α （TNF-α）， reactive oxygen species （ROS） and malondialdehyde （MDA） were detected in gastric mucosa of rats； mRNA expressions of high mobility group box-1 protein （HMGB1） and nuclear factor-κ-B （NF-κB）， relative expressions of nitric oxide synthases （iNOS） and HMGB1， the phosphorylation level of NF-κB p65 were also detected in rats.
RESULTS
2
Compared with normal control group， the DOB value， histopathological score of gastric mucosa， the levels of IL-8， IL-1β， TNF-α， ROS and MDA， relative expressions of HMGB1 and NF-κB mRNA， relative expressions of iNOS and HMGB1 protein and the phosphorylation level of NF-κB p65 were all increased significantly in model group （
P
＜0.05）； the epithelial cells of gastric mucosa in rats were incomplete in structure and decreased in the number， with an increase in cell fragments and vacuoles， and significant cell pyknosis. Compared with model group， the changes of the above indexes in GL groups and positive control group were significantly reversed （
P
＜0.05）； the changes in the above indicators in the GL high-dose group were more significant than GL low-dose and medium-dose groups （
P
＜0.05）； the pathological changes of gastric mucosal cells in rats had all improved.
CONCLUSIONS
2
GL may inhibit inflammation and oxidative stress by inhibiting the activation of HMGB1/NF-κB pathway， thus relieving HP-induced gastric mucosal injury.
关键词
甘草甜素高迁移率族蛋白B1核因子κB幽门螺杆菌相关性胃炎胃黏膜损伤
Keywords
high mobility group box 1 proteinnuclear transcription factor-κBHelicobacter pylori-associated gastritisgastric mucosal injury
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