زرافشان, اقبال ، رهبرقاضی, رضا ، رضایی, جعفر ، اصلانی, محمدرضا ، صابریان پور, شیرین ، احمدی, مهدی ، کیهان منش, رعنا (1400) دیابت نوع دو ازطریق افزایش بیان مولکلولهای چسبندگی اندوتلیال باعث بکارگیری سلول های ایمنی رت به ریه ها می گردد. Advanced Pharmaceutical Bulletin ــ 12 (1). ص.ص.176-182. شاپا 2228-5881
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آدرس اینترنتی رسمی : https://apb.tbzmed.ac.ir/Article/apb-28928
عنوان انگليسی
Type 2 Diabetes Mellitus Provokes Rat Immune Cells Recruitment into the Pulmonary Niche by Up-regulation of Endothelial Adhesion Molecules
خلاصه انگلیسی
Purpose: Diabetes mellitus, especially type 2, is conceived as a devastating chronic metabolic disease globally. Due to the existence of an extensive vascular network in the pulmonary tissue, it is suggested that lungs are sensitive to the diabetic condition like other tissues. This study was designed to address the possible effect of type 2 diabetes mellitus on the promotion of pathological changes via vascular injury. Methods: Sixteen male Wistar rats were randomly allocated to the two of control and T2D groups. To induce type 2 diabetes (T2D), rats were received high-fat and a single dose of streptozotocin (STZ). On week 12, rats were euthanized and lungs samples were taken. Using hematoxylin and eosin (H&E) staining, the pathological changes were monitored. The expression of intercellular adhesion molecule (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), and interleukin 10 (IL-10) was monitored using real-time PCR assay. The level of tumor necrosis factor-α (TNF-α)was detected using ELISA assay. Nitrosative stress was monitored using the Griess assay. Results: Pathological examination in bronchoalveolar discharge revealed the existence of mild to moderate interstitial bronchopneumonia and increased neutrophilic leukocytosis compared to the control. Enhanced ICAM-1 and VCAM-1 expression and suppression of IL-10 was found using real-time PCR analysis (P < 0.05). The levels of TNF-α and NO were increased with diabetic changes compared to the control rats (P < 0.05). Conclusion: T2D could promote pulmonary tissue injury via the production of TNF-α and upregulation of vascular ICAM-1 and VCAM-1. The inflammatory status and vascular ICAM-1 and VCAM-1 increase immune cell recruitment into the pulmonary niche.
نوع سند : | مقاله |
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زبان سند : | انگلیسی |
نویسنده اول : | اقبال زرافشان |
نویسنده : | رضا رهبرقاضی |
نویسنده : | جعفر رضایی |
نویسنده : | محمدرضا اصلانی |
نویسنده : | شیرین صابریان پور |
نویسنده مسئول : | مهدی احمدی |
نویسنده : | رعنا کیهان منش |
ضریب تاثیر و نمایه مجلات: | Indexed in: Scopus, ESCI , PubMed/PMC, Embase |
کلیدواژه ها (انگلیسی): | Type 2 diabetes mellitus, Lungs, Vascular cell adhesion molecules, inflammation,Nitrosative stress |
موضوعات : | WF سیستم تنفسی |
بخش های دانشگاهی : | معاونت تحقیقات و فناوری > مرکز تحقیقاتی علوم دارویی |
کد شناسایی : | 15553 |
ارائه شده توسط : | دکتر محمد رضا اصلانی |
ارائه شده در تاریخ : | 11 اردبهشت 1401 09:06 |
آخرین تغییر : | 11 اردبهشت 1401 09:06 |
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