补体激活靶向抑制剂 C2-FH 可改善对乙酰氨基酚诱发的小鼠肝损伤。

IF 2.5 Q2 GASTROENTEROLOGY & HEPATOLOGY World Journal of Hepatology Pub Date : 2024-10-27 DOI:10.4254/wjh.v16.i10.1188
Chun-Mei Li, Tian Sun, Mou-Jie Yang, Zhi Yang, Qing Li, Jia-Lin Shi, Chong Zhang, Jun-Fei Jin
{"title":"补体激活靶向抑制剂 C2-FH 可改善对乙酰氨基酚诱发的小鼠肝损伤。","authors":"Chun-Mei Li, Tian Sun, Mou-Jie Yang, Zhi Yang, Qing Li, Jia-Lin Shi, Chong Zhang, Jun-Fei Jin","doi":"10.4254/wjh.v16.i10.1188","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Complement activation is recognized as an important factor in the progression of liver damage caused by acetaminophen (APAP). However, the role of the complement inhibitor C2-FH in APAP-induced liver injury remains unclear.</p><p><strong>Aim: </strong>To explore C2-FH in protecting against APAP-induced liver injury by inhibiting complement activation.</p><p><strong>Methods: </strong>A model of APAP-induced liver injury was used to study the protective effect of C2-FH on liver injury. C2-FH was administered through intraperitoneal injection 30 minutes after APAP treatment. We detected the effects of C2-FH on liver function, inflammatory response and complement activation. Additionally, RNA-sequencing (RNA-Seq) analysis was conducted to understand the mechanism through which C2-FH provides protection against APAP-induced liver injury.</p><p><strong>Results: </strong>C2-FH inhibited the increase in serum alanine aminotransferase activity, aspartate aminotransferase activity and lactate dehydrogenase, and reduced liver tissue necrosis caused by APAP. Moreover, it attenuated the inflammatory response and inhibited complement activation in APAP-induced liver injury. RNA-Seq analysis provided additional explanations for the protective role of C2-FH against APAP-induced liver injury.</p><p><strong>Conclusion: </strong>C2-FH attenuates APAP-induced liver injury by inhibiting complement activation.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":2.5000,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11514617/pdf/","citationCount":"0","resultStr":"{\"title\":\"Complement activation targeted inhibitor C2-FH ameliorates acetaminophen-induced liver injury in mice.\",\"authors\":\"Chun-Mei Li, Tian Sun, Mou-Jie Yang, Zhi Yang, Qing Li, Jia-Lin Shi, Chong Zhang, Jun-Fei Jin\",\"doi\":\"10.4254/wjh.v16.i10.1188\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Complement activation is recognized as an important factor in the progression of liver damage caused by acetaminophen (APAP). However, the role of the complement inhibitor C2-FH in APAP-induced liver injury remains unclear.</p><p><strong>Aim: </strong>To explore C2-FH in protecting against APAP-induced liver injury by inhibiting complement activation.</p><p><strong>Methods: </strong>A model of APAP-induced liver injury was used to study the protective effect of C2-FH on liver injury. C2-FH was administered through intraperitoneal injection 30 minutes after APAP treatment. We detected the effects of C2-FH on liver function, inflammatory response and complement activation. Additionally, RNA-sequencing (RNA-Seq) analysis was conducted to understand the mechanism through which C2-FH provides protection against APAP-induced liver injury.</p><p><strong>Results: </strong>C2-FH inhibited the increase in serum alanine aminotransferase activity, aspartate aminotransferase activity and lactate dehydrogenase, and reduced liver tissue necrosis caused by APAP. Moreover, it attenuated the inflammatory response and inhibited complement activation in APAP-induced liver injury. RNA-Seq analysis provided additional explanations for the protective role of C2-FH against APAP-induced liver injury.</p><p><strong>Conclusion: </strong>C2-FH attenuates APAP-induced liver injury by inhibiting complement activation.</p>\",\"PeriodicalId\":23687,\"journal\":{\"name\":\"World Journal of Hepatology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.5000,\"publicationDate\":\"2024-10-27\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11514617/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"World Journal of Hepatology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.4254/wjh.v16.i10.1188\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"GASTROENTEROLOGY & HEPATOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"World Journal of Hepatology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4254/wjh.v16.i10.1188","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"GASTROENTEROLOGY & HEPATOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

背景:补体激活被认为是对乙酰氨基酚(APAP)导致肝损伤进展的一个重要因素。然而,补体抑制剂 C2-FH 在 APAP 诱导的肝损伤中的作用仍不清楚。目的:探讨 C2-FH 通过抑制补体激活对 APAP 诱导的肝损伤的保护作用:方法:使用 APAP 诱导的肝损伤模型研究 C2-FH 对肝损伤的保护作用。在 APAP 治疗 30 分钟后腹腔注射 C2-FH。我们检测了 C2-FH 对肝功能、炎症反应和补体激活的影响。此外,我们还进行了 RNA 序列(RNA-Seq)分析,以了解 C2-FH 保护 APAP 引起的肝损伤的机制:结果:C2-FH抑制了APAP引起的血清丙氨酸氨基转移酶活性、天冬氨酸氨基转移酶活性和乳酸脱氢酶的升高,并减轻了APAP引起的肝组织坏死。此外,在 APAP 诱导的肝损伤中,它还能减轻炎症反应并抑制补体激活。RNA-Seq分析为C2-FH对APAP诱导的肝损伤的保护作用提供了更多解释:结论:C2-FH 可通过抑制补体激活来减轻 APAP 诱导的肝损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Complement activation targeted inhibitor C2-FH ameliorates acetaminophen-induced liver injury in mice.

Background: Complement activation is recognized as an important factor in the progression of liver damage caused by acetaminophen (APAP). However, the role of the complement inhibitor C2-FH in APAP-induced liver injury remains unclear.

Aim: To explore C2-FH in protecting against APAP-induced liver injury by inhibiting complement activation.

Methods: A model of APAP-induced liver injury was used to study the protective effect of C2-FH on liver injury. C2-FH was administered through intraperitoneal injection 30 minutes after APAP treatment. We detected the effects of C2-FH on liver function, inflammatory response and complement activation. Additionally, RNA-sequencing (RNA-Seq) analysis was conducted to understand the mechanism through which C2-FH provides protection against APAP-induced liver injury.

Results: C2-FH inhibited the increase in serum alanine aminotransferase activity, aspartate aminotransferase activity and lactate dehydrogenase, and reduced liver tissue necrosis caused by APAP. Moreover, it attenuated the inflammatory response and inhibited complement activation in APAP-induced liver injury. RNA-Seq analysis provided additional explanations for the protective role of C2-FH against APAP-induced liver injury.

Conclusion: C2-FH attenuates APAP-induced liver injury by inhibiting complement activation.

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
World Journal of Hepatology
World Journal of Hepatology GASTROENTEROLOGY & HEPATOLOGY-
CiteScore
4.10
自引率
4.20%
发文量
172
期刊最新文献
Chronic hepatitis B: Prevent, diagnose, and treat before the point of no return. Complement activation targeted inhibitor C2-FH ameliorates acetaminophen-induced liver injury in mice. Hepatitis B surface antigen-negative but hepatitis B envelope antigen-positive false occult hepatitis B virus infection: A case report. Liver cell cancer surveillance practice in Nigeria: Pitfalls and future prospects. Pathogenesis and research progress of nonalcoholic fatty liver disease/nonalcoholic steatohepatitis.
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1