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

刘誉华; 刘莲; 汪九重; 黄丹; 周素芳; 肖欢智; 安祯祥

doi:10.6039/j.issn.1001-0408.2024.02.08

您当前的位置：

首页 >

文章列表页 >

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

药学研究 | 更新时间：2024-01-24

- 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
- Improvement effects of glycyrrhizin on Helicobacter pylori-associated gastritis in rats and its mechanism
- 中国药房 2024年35卷第2期页码：166-171
- 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：
  
  副主任医师，博士研究生。研究方向：中医药防治脾胃病。电话：0851-85636327。E-mail：394717866@qq.com
  主任医师，博士生导师，博士。研究方向：中医药防治脾胃病、肝病。电话：0851-85636327。E-mail：407206115@qq.com
- 基金信息：
  
  贵州省科技计划项目(黔科合支撑〔2020〕4Y077号);贵州省卫生健康委科学技术基金项目(gzwkj2023-139);贵州中医药大学国家与省级科技创新人才团队培育项目(贵中医TD合字〔2022〕005号)
- DOI：10.6039/j.issn.1001-0408.2024.02.08
  中图分类号： R965;R285.5
- 纸质出版日期：2024-01-30，
  
  收稿日期：2023-05-10，
  
  修回日期：2023-12-27，
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

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

以接种1×10

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

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

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（

＜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（

＜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（

＜0.05）；大鼠胃黏膜细胞病理变化均改善。

结论

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

To investigate the improvement effects of glycyrrhizin （GL） on

Helicobacter pylori

（HP）-associated gastritis in rats and its mechanism.

METHODS

HP-associated gastritis rat model was induced by inoculating with 1×10

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

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

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 （

＜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 （

＜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 （

＜0.05）； the pathological changes of gastric mucosal cells in rats had all improved.

CONCLUSIONS

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

references

HOOI J K Y，LAI W Y，NG W K，et al. Global prevalence of Helicobacter pylori infection：systematic review and meta-analysis[J]. Gastroenterology，2017，153（2）：420-429.

QIONG H，HAN L，ZHANG N X，et al. Glycyrrhizin improves the pathogenesis of psoriasis partially through IL-17A and the SIRT1-STAT3 axis[J]. BMC Immunol，2021，22（1）：34.

LIN H J，HSU F Y，CHEN W W，et al. Helicobacter pylori activates HMGB1 expression and recruits RAGE into lipid rafts to promote inflammation in gastric epithelial cells[J]. Front Immunol，2016，7：341.

YU R Q，JIANG S Y，TAO Y Q，et al. Inhibition of HMGB1 improves necrotizing enterocolitis by inhibiting NLRP3 via TLR4 and NF-κB signaling pathways[J]. J Cell Physiol，2019，234（8）：13431-13438.

WEN J X，WU S H，MA X，et al. Zuojin Pill attenuates Helicobacter pylori-induced chronic atrophic gastritis in rats and improves gastric epithelial cells function in GES-1 cells[J]. J Ethnopharmacol，2022，285：114855.

KHAN U，KARMAKAR B C，BASAK P，et al. Glycyrrhizin，an inhibitor of HMGB1 induces autolysosomal degradation function and inhibits Helicobacter pylori infection[J]. Mol Med，2023，29（1）：51.

刘婉琼，董礼刚，尤佳，等. 健脾清化汤对幽门螺杆菌相关性胃炎大鼠胃黏膜HSP70/NF-κB信号通路的影响[J]. 中华中医药杂志，2021，36（8）：4969-4972.

LIU W Q，DONG L G，YOU J，et al. Effects of Jianpi Qing-hua Decoction on HSP70/NF-κB signal pathway of ga-stric mucosa in rats with Helicobacter pylori-associated gastritis[J]. China J Tradit Chin Med Pharm，2021，36（8）：4969-4972.

HU Z H，XIAO M，CAI H X，et al. Glycyrrhizin regulates rat TMJOA progression by inhibiting the HMGB1-RAGE/TLR4-NF-κB/AKT pathway[J]. J Cell Mol Med，2022，26（3）：925-936.

吴德坤，唐友明，郑景辉，等. 安胃汤对幽门螺旋杆菌阳性萎缩性胃炎模型大鼠保护作用的药理探索[J]. 中药新药与临床药理，2022，33（1）：57-63.

WU D K，TANG Y M，ZHENG J H，et al. Pharmacologic study of anwei decoction on the protection of atrophic chronic gastritis rats with Helicobacter pylori positive[J]. Tradit Chin Drug Res Clin Pharmacol，2022，33（1）：57-63.

江明礼，莫非，渠巍，等. 苗药头花蓼对感染幽门螺杆菌胃炎细胞TLRs信号通路的影响[J]. 贵州医科大学学报，2019，44（2）：184-189.

JIANG M L，MO F，QU W，et al. Effect of Polygonum capitatum on TLRs signal pathway in Helicobacter pylori gastritis cells[J]. J Guizhou Med Univ，2019，44（2）：184-189.

KIM H S，LIM J W，KIM H. Korean red ginseng extract inhibits IL-8 expression via Nrf2 activation in Helicobacter pylori-infected gastric epithelial cells[J]. Nutrients，2022，14（5）：1044.

TIWARI S K，SHAIK A S，SHAIK A P，et al. Gene expression patterns of COX-1，COX-2 and iNOS in H. pylori infected histopathological conditions[J]. Microb Pathog，2019，135：103634.

SIRIVIRIYAKUL P，WERAWATGANON D，PHETNOO N，et al. Genistein attenuated gastric inflammation and apoptosis in Helicobacter pylori-induced gastropathy in rats[J]. BMC Gastroenterol，2020，20（1）：410.

SHEN C H，MA Z Y，LI J H，et al. Glycyrrhizin improves inflammation and apoptosis via suppressing HMGB1 and PI3K/mTOR pathway in lipopolysaccharide-induced acute liver injury[J]. Eur Rev Med Pharmacol Sci，2020，24（12）：7122-7130.

浏览量

下载量

CSCD

文章被引用时，请邮件提醒。

提交

工具集

关联资源

暂无数据