این سایت در حال حاضر پشتیبانی نمی شود و امکان دارد داده های نشریات بروز نباشند
Iranian Journal of Basic Medical Sciences، جلد ۲۶، شماره ۳، صفحات ۳۷۴-۳۷۹
عنوان فارسی
چکیده فارسی مقاله
کلیدواژه‌های فارسی مقاله
عنوان انگلیسی 11β-Hydroxysteroid dehydrogenase type 1 amplifies inflammation in LPS-induced THP-1 cells
چکیده انگلیسی مقاله Objective(s): The role of glucocorticoids as anti-inflammatory and immune-stimulatory drugs has been widely reported. However, the role of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), which catalyzes the conversion of inactive cortisone into active cortisol, in inflammation remains unclear. This study aimed to examine the mechanism of actions of 11β-HSD1 in lipopolysaccharide (LPS)-induced THP-1 cells.Materials and Methods: The gene expression of 11β-HSD1 and pro-inflammatory cytokines was detected via RT-PCR. The protein expression of IL-1β in cell supernatants was detected via ELISA. Oxidative stress and mitochondrial membrane potential were assessed using a reactive oxygen species (ROS) kit and a mitochondrial membrane potential (MMP) kit, respectively. The expression of Nuclear Factor- Kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) was detected via western blotting.Results: Elevated levels of 11β-HSD1 contributed to the expression of inflammatory cytokines, whereas BVT.2733, a selective 11β-HSD1 inhibitor, ameliorated inflammatory responses, ROS, and mitochondrial damage in LPS-stimulated THP-1 cells. Furthermore, cortisone and cortisol, which are the substrate and product of 11β-HSD1, respectively, showed biphasic responses and induced the expression of pro-inflammatory cytokines at a low concentration in both LPS-stimulated or untreated THP-1 cells. The enhanced inflammation was attenuated by co-treatment with BVT.2733 and the glucocorticoid receptor (GR) antagonist RU486, but not in those treated with the mineralocorticoid receptor (MR) antagonist spironolactone. Overall, the results indicate that 11β-HSD1 amplifies inflammatory responses by activating the NF-κB and MAPK signaling pathways.Conclusion: Inhibition of 11β-HSD1 may serve as a potential therapeutic target against the excessive activation of inflammation.
کلیدواژه‌های انگلیسی مقاله 11β-Hydroxysteroid- dehydrogenase type 1, BVT.2733, Glucocorticoid Inflammation, THP-1 cells
نویسندگان مقاله | Lingli Luo
Department of Geriatrics Intensive Care Unit, The First Affiliated Hospital of Nanjing Medical University. NO.300 Guangzhou Road, Nanjing, 210029, Jiangsu Province, China


| Dongmei Zhu
Department of Geriatrics Intensive Care Unit, The First Affiliated Hospital of Nanjing Medical University. NO.300 Guangzhou Road, Nanjing, 210029, Jiangsu Province, China


| Zheng Zhang
Department of Geriatrics Intensive Care Unit, The First Affiliated Hospital of Nanjing Medical University. NO.300 Guangzhou Road, Nanjing, 210029, Jiangsu Province, China


| Hanjie Zeng
Department of Geriatrics Intensive Care Unit, The First Affiliated Hospital of Nanjing Medical University. NO.300 Guangzhou Road, Nanjing, 210029, Jiangsu Province, China


| Min Huang
Department of Geriatrics Intensive Care Unit, The First Affiliated Hospital of Nanjing Medical University. NO.300 Guangzhou Road, Nanjing, 210029, Jiangsu Province, China


| Suming Zhou
Department of Geriatrics Intensive Care Unit, The First Affiliated Hospital of Nanjing Medical University. NO.300 Guangzhou Road, Nanjing, 210029, Jiangsu Province, China
نشانی اینترنتی https://ijbms.mums.ac.ir/article_21729.html
فایل مقاله فایلی برای مقاله ذخیره نشده است
کد مقاله (doi)
زبان مقاله منتشر شده en
موضوعات مقاله منتشر شده
نوع مقاله منتشر شده Original Article
برگشت به: صفحه اول پایگاه   |   نسخه مرتبط   |   نشریه مرتبط   |   فهرست نشریات