[黄芩汤通过降低内质网应激减轻小鼠溃疡性结肠炎]。

Q3 Medicine
J Qiu, Y Qiu, G Li, L Zhang, X Zheng, Y Yao, X Wang, H Huang, F Zhang, J Su, X Zheng, X Huang
{"title":"[黄芩汤通过降低内质网应激减轻小鼠溃疡性结肠炎]。","authors":"J Qiu, Y Qiu, G Li, L Zhang, X Zheng, Y Yao, X Wang, H Huang, F Zhang, J Su, X Zheng, X Huang","doi":"10.12122/j.issn.1673-4254.2024.11.14","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To evaluate the therapeutic effect of <i>Huangqin</i> Decoction (HQD) on ulcerative colitis (UC) in mice and explore its mechanism.</p><p><strong>Methods: </strong>Male Balb/c mice were randomly divided into normal control group, model group, mesalazine group (5-ASA, 200 mg/kg), and low-, medium-and high-dose HQD groups (2.275, 4.55 and 9.1 g/kg, respectively). With the exception of those in the normal control group, all the mice were exposed to 3% DSS solution in drinking water for 7 days to establish UC models. After treatment with the indicated drugs, the mice were assessed for colon injury and apoptosis using HE, AB-PAS and TUNEL staining, and the expression levels of inflammatory factors were detected with ELISA. Western blotting, immunohistochemistry and qRT-PCR were used to detect the changes in protein expressions associated with the intestinal chemical barrier, mechanical barrier and endoplasmic reticulum stress (ERS).</p><p><strong>Results: </strong>HQD treatment significantly reduced DAI score and macro score of UC mice, decreased colonic epithelial cell apoptosis, lowered expressions of IL-6, TNF-α, IL-1β and IL-8, and enhanced the expressions of MUC2 and TFF3. HQD treatment also upregulated the protein expressions of claudin-1, occludin and E-cadherin, reduced the expressions of GRP78, CHOP, caspase-12 and caspase-3, decreased the phosphorylation levels of PERK, eIF2α and IRE1α, and increased the Bcl-2/Bax ratio in the colon tissues of UC mice.</p><p><strong>Conclusion: </strong>HQD inhibits colonic epithelial cell apoptosis and improves intestinal barrier function in UC mice possibly by reducing ERS mediated by the PERK and IRE1α signaling pathways.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"44 11","pages":"2172-2183"},"PeriodicalIF":0.0000,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11605200/pdf/","citationCount":"0","resultStr":"{\"title\":\"[<i>Huangqin</i> Decoction alleviates ulcerative colitis in mice by reducing endoplasmic reticulum stress].\",\"authors\":\"J Qiu, Y Qiu, G Li, L Zhang, X Zheng, Y Yao, X Wang, H Huang, F Zhang, J Su, X Zheng, X Huang\",\"doi\":\"10.12122/j.issn.1673-4254.2024.11.14\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>To evaluate the therapeutic effect of <i>Huangqin</i> Decoction (HQD) on ulcerative colitis (UC) in mice and explore its mechanism.</p><p><strong>Methods: </strong>Male Balb/c mice were randomly divided into normal control group, model group, mesalazine group (5-ASA, 200 mg/kg), and low-, medium-and high-dose HQD groups (2.275, 4.55 and 9.1 g/kg, respectively). With the exception of those in the normal control group, all the mice were exposed to 3% DSS solution in drinking water for 7 days to establish UC models. After treatment with the indicated drugs, the mice were assessed for colon injury and apoptosis using HE, AB-PAS and TUNEL staining, and the expression levels of inflammatory factors were detected with ELISA. Western blotting, immunohistochemistry and qRT-PCR were used to detect the changes in protein expressions associated with the intestinal chemical barrier, mechanical barrier and endoplasmic reticulum stress (ERS).</p><p><strong>Results: </strong>HQD treatment significantly reduced DAI score and macro score of UC mice, decreased colonic epithelial cell apoptosis, lowered expressions of IL-6, TNF-α, IL-1β and IL-8, and enhanced the expressions of MUC2 and TFF3. HQD treatment also upregulated the protein expressions of claudin-1, occludin and E-cadherin, reduced the expressions of GRP78, CHOP, caspase-12 and caspase-3, decreased the phosphorylation levels of PERK, eIF2α and IRE1α, and increased the Bcl-2/Bax ratio in the colon tissues of UC mice.</p><p><strong>Conclusion: </strong>HQD inhibits colonic epithelial cell apoptosis and improves intestinal barrier function in UC mice possibly by reducing ERS mediated by the PERK and IRE1α signaling pathways.</p>\",\"PeriodicalId\":18962,\"journal\":{\"name\":\"南方医科大学学报杂志\",\"volume\":\"44 11\",\"pages\":\"2172-2183\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-11-20\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11605200/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"南方医科大学学报杂志\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.12122/j.issn.1673-4254.2024.11.14\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"南方医科大学学报杂志","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.12122/j.issn.1673-4254.2024.11.14","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0

摘要

目的:评价黄芩汤对小鼠溃疡性结肠炎的治疗作用,并探讨其作用机制。方法:将雄性Balb/c小鼠随机分为正常对照组、模型组、美沙嗪组(5-ASA, 200 mg/kg)和HQD低、中、高剂量组(分别为2.275、4.55、9.1 g/kg)。除正常对照组外,其余小鼠均在饮用水中添加3% DSS溶液,连续7 d建立UC模型。给药后,采用HE、AB-PAS、TUNEL染色检测小鼠结肠损伤及凋亡情况,ELISA检测炎症因子表达水平。采用Western blotting、免疫组织化学和qRT-PCR检测肠道化学屏障、机械屏障和内质网应激(endoplasmic reticulum stress, ERS)相关蛋白的表达变化。结果:HQD治疗显著降低UC小鼠DAI评分和宏观评分,减少结肠上皮细胞凋亡,降低IL-6、TNF-α、IL-1β、IL-8表达,增强MUC2、TFF3表达。HQD还上调了UC小鼠结肠组织中claudin-1、occludin和E-cadherin的蛋白表达,降低了GRP78、CHOP、caspase-12和caspase-3的表达,降低了PERK、eIF2α和IRE1α的磷酸化水平,增加了Bcl-2/Bax比值。结论:HQD可能通过降低PERK和IRE1α信号通路介导的ERS,抑制UC小鼠结肠上皮细胞凋亡,改善肠道屏障功能。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Huangqin Decoction alleviates ulcerative colitis in mice by reducing endoplasmic reticulum stress].

Objective: To evaluate the therapeutic effect of Huangqin Decoction (HQD) on ulcerative colitis (UC) in mice and explore its mechanism.

Methods: Male Balb/c mice were randomly divided into normal control group, model group, mesalazine group (5-ASA, 200 mg/kg), and low-, medium-and high-dose HQD groups (2.275, 4.55 and 9.1 g/kg, respectively). With the exception of those in the normal control group, all the mice were exposed to 3% DSS solution in drinking water for 7 days to establish UC models. After treatment with the indicated drugs, the mice were assessed for colon injury and apoptosis using HE, AB-PAS and TUNEL staining, and the expression levels of inflammatory factors were detected with ELISA. Western blotting, immunohistochemistry and qRT-PCR were used to detect the changes in protein expressions associated with the intestinal chemical barrier, mechanical barrier and endoplasmic reticulum stress (ERS).

Results: HQD treatment significantly reduced DAI score and macro score of UC mice, decreased colonic epithelial cell apoptosis, lowered expressions of IL-6, TNF-α, IL-1β and IL-8, and enhanced the expressions of MUC2 and TFF3. HQD treatment also upregulated the protein expressions of claudin-1, occludin and E-cadherin, reduced the expressions of GRP78, CHOP, caspase-12 and caspase-3, decreased the phosphorylation levels of PERK, eIF2α and IRE1α, and increased the Bcl-2/Bax ratio in the colon tissues of UC mice.

Conclusion: HQD inhibits colonic epithelial cell apoptosis and improves intestinal barrier function in UC mice possibly by reducing ERS mediated by the PERK and IRE1α signaling pathways.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
南方医科大学学报杂志
南方医科大学学报杂志 Medicine-Medicine (all)
CiteScore
1.50
自引率
0.00%
发文量
208
期刊介绍:
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信