阻断杏仁蛋白受体 (APJ) 可减轻 TNBS 诱发的大鼠结肠炎

IF 0.3 Q3 MEDICINE, GENERAL & INTERNAL
I. Birsen, Osman Sinen, Simla Su Akkan, I. Üstünel, V. İzgüt-Uysal, Prof. Dr. V. Nimet, Simla Su, PhD Akkan
{"title":"阻断杏仁蛋白受体 (APJ) 可减轻 TNBS 诱发的大鼠结肠炎","authors":"I. Birsen, Osman Sinen, Simla Su Akkan, I. Üstünel, V. İzgüt-Uysal, Prof. Dr. V. Nimet, Simla Su, PhD Akkan","doi":"10.58600/eurjther1883","DOIUrl":null,"url":null,"abstract":"Objective: The apelinergic system, consisting of apelin, ELABELA, and the apelin receptor (APJ), has a wide range of roles in physiological and pathophysiological processes in tissues. The effects of increased apelin and APJ as an indicator of damage in inflammatory conditions or as a compensatory mechanism are not fully clear in inflammatory bowel disease (IBD). This study was designed to assess the role of APJ in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model. Methods: Colitis in adult male Wistar rats were induced by intrarectally administered TNBS (30 mg b.w. in 50% ethanol). While the control group was treated with only saline to the colon, the TNBS+F13A and F13A groups received the APJ antagonist F13A (30 µg/kg/day, i.v.) for 3 days, starting immediately after TNBS or saline administration, respectively. Results: A decrease in body weight and an increase in colon weight/length ratio and stool consistency score were observed in the TNBS group. TNBS caused an increase in the myeloperoxidase (MPO) activity and the number of proinflammatory cytokines (TNF-α, IL-1β, and IL-6), as well as apelin production, leading to mucosal ulceration, necrosis, and submucosal edema in the colon. While F13A administration to the control did not cause any change in the colon, F13A administration immediately after TNBS greatly reduced the effects of TNBS. Conclusion: APJ is involved in the development of damage in colitis induced by TNBS. F13A reduces the level of damage, inflammatory cell infiltration, and MPO enzyme activity. APJ may be a therapeutic target in IBD.","PeriodicalId":42642,"journal":{"name":"European Journal of Therapeutics","volume":null,"pages":null},"PeriodicalIF":0.3000,"publicationDate":"2023-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Blocking the Apelin Receptor (APJ) Attenuates TNBS-Induced Colitis in Rats\",\"authors\":\"I. Birsen, Osman Sinen, Simla Su Akkan, I. Üstünel, V. İzgüt-Uysal, Prof. Dr. V. Nimet, Simla Su, PhD Akkan\",\"doi\":\"10.58600/eurjther1883\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Objective: The apelinergic system, consisting of apelin, ELABELA, and the apelin receptor (APJ), has a wide range of roles in physiological and pathophysiological processes in tissues. The effects of increased apelin and APJ as an indicator of damage in inflammatory conditions or as a compensatory mechanism are not fully clear in inflammatory bowel disease (IBD). This study was designed to assess the role of APJ in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model. Methods: Colitis in adult male Wistar rats were induced by intrarectally administered TNBS (30 mg b.w. in 50% ethanol). While the control group was treated with only saline to the colon, the TNBS+F13A and F13A groups received the APJ antagonist F13A (30 µg/kg/day, i.v.) for 3 days, starting immediately after TNBS or saline administration, respectively. Results: A decrease in body weight and an increase in colon weight/length ratio and stool consistency score were observed in the TNBS group. TNBS caused an increase in the myeloperoxidase (MPO) activity and the number of proinflammatory cytokines (TNF-α, IL-1β, and IL-6), as well as apelin production, leading to mucosal ulceration, necrosis, and submucosal edema in the colon. While F13A administration to the control did not cause any change in the colon, F13A administration immediately after TNBS greatly reduced the effects of TNBS. Conclusion: APJ is involved in the development of damage in colitis induced by TNBS. F13A reduces the level of damage, inflammatory cell infiltration, and MPO enzyme activity. APJ may be a therapeutic target in IBD.\",\"PeriodicalId\":42642,\"journal\":{\"name\":\"European Journal of Therapeutics\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.3000,\"publicationDate\":\"2023-11-20\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"European Journal of Therapeutics\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.58600/eurjther1883\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"MEDICINE, GENERAL & INTERNAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"European Journal of Therapeutics","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.58600/eurjther1883","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
引用次数: 0

摘要

目的:凋亡素能系统由凋亡素、ELABELA和凋亡素受体(APJ)组成,在组织的生理和病理生理过程中发挥着广泛的作用。在炎症性肠病(IBD)中,杏仁蛋白和 APJ 的增加是炎症条件下的损伤指标,还是一种代偿机制,其作用尚不完全清楚。本研究旨在评估 APJ 在 2,4,6-三硝基苯磺酸(TNBS)诱导的结肠炎模型中的作用。研究方法通过直肠给药 TNBS(30 毫克体重,50% 乙醇)诱导成年雄性 Wistar 大鼠结肠炎。对照组仅用生理盐水灌肠,TNBS+F13A 组和 F13A 组分别在 TNBS 或生理盐水给药后立即开始接受 APJ 拮抗剂 F13A(30 µg/kg/天,静脉注射)治疗 3 天。研究结果TNBS 组的体重下降,结肠重量/长度比和粪便稠度评分增加。TNBS 导致髓过氧化物酶 (MPO) 活性和促炎细胞因子(TNF-α、IL-1β 和 IL-6)数量以及凋亡素生成增加,从而导致结肠粘膜溃疡、坏死和粘膜下水肿。对照组服用 F13A 不会导致结肠发生任何变化,而在 TNBS 结束后立即服用 F13A 则会大大减轻 TNBS 的影响。结论APJ 参与了 TNBS 诱导的结肠炎损伤的发展。F13A 可降低损伤程度、炎症细胞浸润和 MPO 酶活性。APJ 可能是 IBD 的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Blocking the Apelin Receptor (APJ) Attenuates TNBS-Induced Colitis in Rats
Objective: The apelinergic system, consisting of apelin, ELABELA, and the apelin receptor (APJ), has a wide range of roles in physiological and pathophysiological processes in tissues. The effects of increased apelin and APJ as an indicator of damage in inflammatory conditions or as a compensatory mechanism are not fully clear in inflammatory bowel disease (IBD). This study was designed to assess the role of APJ in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model. Methods: Colitis in adult male Wistar rats were induced by intrarectally administered TNBS (30 mg b.w. in 50% ethanol). While the control group was treated with only saline to the colon, the TNBS+F13A and F13A groups received the APJ antagonist F13A (30 µg/kg/day, i.v.) for 3 days, starting immediately after TNBS or saline administration, respectively. Results: A decrease in body weight and an increase in colon weight/length ratio and stool consistency score were observed in the TNBS group. TNBS caused an increase in the myeloperoxidase (MPO) activity and the number of proinflammatory cytokines (TNF-α, IL-1β, and IL-6), as well as apelin production, leading to mucosal ulceration, necrosis, and submucosal edema in the colon. While F13A administration to the control did not cause any change in the colon, F13A administration immediately after TNBS greatly reduced the effects of TNBS. Conclusion: APJ is involved in the development of damage in colitis induced by TNBS. F13A reduces the level of damage, inflammatory cell infiltration, and MPO enzyme activity. APJ may be a therapeutic target in IBD.
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
European Journal of Therapeutics
European Journal of Therapeutics MEDICINE, GENERAL & INTERNAL-
自引率
0.00%
发文量
48
×
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