{"title":"西格列汀调节 RAW 264.7 巨噬细胞中的炎症指标和 LPS 加重 CFA 诱导的大鼠类风湿性关节炎","authors":"A. B. Ahmed, Purbajit Chetia","doi":"10.15584/ejcem.2024.1.12","DOIUrl":null,"url":null,"abstract":"Introduction and aim. Rheumatoid arthritis (RA) causes pain, inflammation, and deformities in numerous joints. Monoamine oxidase B (MOA-B) inhibitor selegiline exhibits anti-inflammatory characteristics and has the propensity to scavenge free radicals. Therefore, the aim of this research comprises of assessing the effect of selegiline on proinflammatory cytokines in RAW 264.7 macrophages as well as its capacity to improve various arthritic parameters in rats with lipopolysaccharide (LPS) accelerated complete Freund’s adjuvant (CFA) induced RA. Material and methods. In RAW 264.7 cells (lipopolysaccharide accelerated), nitric oxide (NO), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), inducible nitric oxide synthase (iNOS), and prostaglandin E2 (PGE2 ) were determined after treat ment with selegiline. Different arthritic parameters were analyzed after administration of selegiline in LPS accelerated CFA-induced arthritis in rats. Results. LPS escalates NO, TNF-α, IL-6, iNOS, and PGE2 quantities in the RAW 264.7 cells, which was minimized by selegiline at 100 µg/mL and 150 µg/mL respectively. In rats, CFA induction causes a decrease in body weight, elevation of paw volume, splenic index, and arthritic index, which are further accelerated by LPS. 20 mg/kg of selegiline managed all these arthritic parameters effectively, including TNF-α, IL-6, and a few other biochemical parameters. Conclusion. Selegiline may be beneficial in RA extenuating joint and cartilage damage, and modulating inflammatory responses.","PeriodicalId":11828,"journal":{"name":"European Journal of Clinical and Experimental Medicine","volume":"41 8","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Selegiline modulates inflammatory indicators in RAW 264.7 macrophages and LPS-aggravated CFA-induced rheumatoid arthritis in rats\",\"authors\":\"A. B. Ahmed, Purbajit Chetia\",\"doi\":\"10.15584/ejcem.2024.1.12\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Introduction and aim. Rheumatoid arthritis (RA) causes pain, inflammation, and deformities in numerous joints. Monoamine oxidase B (MOA-B) inhibitor selegiline exhibits anti-inflammatory characteristics and has the propensity to scavenge free radicals. Therefore, the aim of this research comprises of assessing the effect of selegiline on proinflammatory cytokines in RAW 264.7 macrophages as well as its capacity to improve various arthritic parameters in rats with lipopolysaccharide (LPS) accelerated complete Freund’s adjuvant (CFA) induced RA. Material and methods. In RAW 264.7 cells (lipopolysaccharide accelerated), nitric oxide (NO), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), inducible nitric oxide synthase (iNOS), and prostaglandin E2 (PGE2 ) were determined after treat ment with selegiline. Different arthritic parameters were analyzed after administration of selegiline in LPS accelerated CFA-induced arthritis in rats. Results. LPS escalates NO, TNF-α, IL-6, iNOS, and PGE2 quantities in the RAW 264.7 cells, which was minimized by selegiline at 100 µg/mL and 150 µg/mL respectively. In rats, CFA induction causes a decrease in body weight, elevation of paw volume, splenic index, and arthritic index, which are further accelerated by LPS. 20 mg/kg of selegiline managed all these arthritic parameters effectively, including TNF-α, IL-6, and a few other biochemical parameters. Conclusion. Selegiline may be beneficial in RA extenuating joint and cartilage damage, and modulating inflammatory responses.\",\"PeriodicalId\":11828,\"journal\":{\"name\":\"European Journal of Clinical and Experimental Medicine\",\"volume\":\"41 8\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-03-30\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"European Journal of Clinical and Experimental Medicine\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.15584/ejcem.2024.1.12\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"European Journal of Clinical and Experimental Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.15584/ejcem.2024.1.12","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
导言和目的。类风湿性关节炎(RA)会导致许多关节疼痛、发炎和畸形。单胺氧化酶 B(MOA-B)抑制剂西格列汀具有抗炎特性和清除自由基的倾向。因此,本研究旨在评估西格列汀对 RAW 264.7 巨噬细胞中的促炎细胞因子的影响,以及其改善脂多糖(LPS)加速完全弗氏佐剂(CFA)诱导的大鼠 RA 的各种关节炎参数的能力。材料与方法使用西格列汀治疗后,测定 RAW 264.7 细胞(脂多糖加速)中的一氧化氮(NO)、肿瘤坏死因子α(TNF-α)、白细胞介素 6(IL-6)、诱导型一氧化氮合酶(iNOS)和前列腺素 E2(PGE2)。在 LPS 加速 CFA 诱导的大鼠关节炎中使用西格列汀后,对不同的关节炎参数进行了分析。结果显示LPS 使 RAW 264.7 细胞中的 NO、TNF-α、IL-6、iNOS 和 PGE2 数量增加,西格列汀分别以 100 微克/毫升和 150 微克/毫升的剂量将其降到最低。在大鼠体内,CFA 诱导会导致体重下降、爪体积增大、脾指数和关节炎指数升高,而 LPS 会进一步加速这些变化。20 毫克/千克的西格列汀可有效控制所有这些关节炎指标,包括 TNF-α、IL-6 和其他一些生化指标。结论西格列汀对减轻关节和软骨损伤、调节炎症反应可能有益。
Selegiline modulates inflammatory indicators in RAW 264.7 macrophages and LPS-aggravated CFA-induced rheumatoid arthritis in rats
Introduction and aim. Rheumatoid arthritis (RA) causes pain, inflammation, and deformities in numerous joints. Monoamine oxidase B (MOA-B) inhibitor selegiline exhibits anti-inflammatory characteristics and has the propensity to scavenge free radicals. Therefore, the aim of this research comprises of assessing the effect of selegiline on proinflammatory cytokines in RAW 264.7 macrophages as well as its capacity to improve various arthritic parameters in rats with lipopolysaccharide (LPS) accelerated complete Freund’s adjuvant (CFA) induced RA. Material and methods. In RAW 264.7 cells (lipopolysaccharide accelerated), nitric oxide (NO), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), inducible nitric oxide synthase (iNOS), and prostaglandin E2 (PGE2 ) were determined after treat ment with selegiline. Different arthritic parameters were analyzed after administration of selegiline in LPS accelerated CFA-induced arthritis in rats. Results. LPS escalates NO, TNF-α, IL-6, iNOS, and PGE2 quantities in the RAW 264.7 cells, which was minimized by selegiline at 100 µg/mL and 150 µg/mL respectively. In rats, CFA induction causes a decrease in body weight, elevation of paw volume, splenic index, and arthritic index, which are further accelerated by LPS. 20 mg/kg of selegiline managed all these arthritic parameters effectively, including TNF-α, IL-6, and a few other biochemical parameters. Conclusion. Selegiline may be beneficial in RA extenuating joint and cartilage damage, and modulating inflammatory responses.