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مقالات فارسیISIکنفرانسهاژورنالها

S۱۰۰A۹ aggravates bleomycin-induced dermal fibrosis in mice via activation of ERK۱/۲ MAPK and NF-κB pathways

محل انتشار: مجله علوم پایه پزشکی ایران، دوره: 21، شماره: 2
سال انتشار: 1397
نوع سند: مقاله ژورنالی
زبان: انگلیسی
مشاهده: 197

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استخراج به نرم افزارهای پژوهشی:

لینک ثابت به این مقاله:
https://civilica.com/doc/1295381

شناسه ملی سند علمی:

JR_IJBMS-21-2_012

تاریخ نمایه سازی: 27 مهر 1400

چکیده مقاله:

Objective(s): This study aims to investigate the pathogenicity and possible mechanisms of S۱۰۰A۹ function in mice models of scleroderma. Materials and Methods: The content of S۱۰۰A۹ in the skin tissues of mice with scleroderma was determined. Different concentrations of bleomycin (BLM) and S۱۰۰A۹ were subcutaneously injected into the backs of mice simultaneously, and then pathological changes in the skin of these mice were monitored. Specifically, the levels of inflammatory cytokines and alpha smooth muscle actin (α-SMA), the activation of extracellular regulated kinase ۱/۲ (ERK۱/۲), mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) pathways, and the expression of the receptor for advanced glycation end-product (RAGE) in the skin were determined. Results: The content of S۱۰۰A۹ in the skin tissues of mice with scleroderma was determined. Different concentrations of BLM and S۱۰۰A۹ were subcutaneously injected into the backs of mice simultaneously, and then pathological changes in the skin of these mice were monitored. Specifically, the levels of inflammatory cytokines and alpha smooth muscle actin (α-SMA), the activation of extracellular regulated kinase ۱/۲ (ERK۱/۲) mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) pathways, and the expression of the receptor for advanced glycation end-product (RAGE) in the skin were determined. Conclusion: S۱۰۰A۹ aggravates dermal fibrosis in BLM-induced scleroderma (BIS ) mice, and its mechanisms might be mediated by RAGE, ERK۱/۲, and NF-κB pathway.

کلیدواژه ها:

S۱۰۰A۹ ، Scleroderma ، Bleomycin ، RAGE ، ERK۱/۲ MAPK ، NF-κB

نویسندگان

Xue Xu

Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing ۲۱۰۰۰۸, Jiangsu, China

Zhiyong Chen

Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing ۲۱۰۰۰۸, Jiangsu, China

Xiaoxia Zhu

Division of Rheumatology, Huashan Hospital, Fudan University, Shanghai ۲۰۰۰۴۰, China

Dandan Wang

Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing ۲۱۰۰۰۸, Jiangsu, China

Jun Liang

Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing ۲۱۰۰۰۸, Jiangsu, China

Cheng Zhao

Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing ۲۱۰۰۰۸, Jiangsu, China

Xuebing Feng

Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing ۲۱۰۰۰۸, Jiangsu, China

Jiucun Wang

State Key Laboratory of Genetic Engineering and Ministry of Education Key Laboratory of Contemporary Anthropology, School of Life Sciences, Fudan University, Shanghai ۲۰۰۴۳۳, China

Hejian Zou

Division of Rheumatology, Huashan Hospital, Fudan University, Shanghai ۲۰۰۰۴۰, China

Lingyun Sun

Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing ۲۱۰۰۰۸, Jiangsu, China

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