间充质干细胞
炎症性肠病
医学
白细胞介素
HMGB1
白细胞介素17
炎症体
发病机制
免疫学
促炎细胞因子
炎症
肿瘤坏死因子α
内科学
细胞因子
病理
疾病
作者
Shuzan Ali Mohammed,Azza Elbaramawy,Somia H. Abd‐Allah,Adel El-Kholy,N. Elsayed,Samia Hussein
摘要
Abstract Interleukin‐1beta (IL‐1β) and interleukin‐17A (IL‐17A) have strong pro‐inflammatory activities that are involved in inflammatory bowel diseases (IBDs). Mesenchymal stem cell (MSC) therapy is considered a promising treatment for IBD. This study was performed to understand the role of rat Nlrp3 inflammasome, Hmgb1 , and pro‐inflammatory cytokines (IL‐1β and IL‐17a) in the pathogenesis of IBD. Also, to evaluate the role of human umbilical cord blood‐MSCs (hUCB‐MSCs) in the management of IBD. The rats were in four groups: normal controls, indomethacin‐induced IBD group, indomethacin‐induced IBD rats that received phosphate‐buffered saline (PBS), and the IBD group that received hUCB‐MSCs as a treatment. The messenger RNA (mRNA) expression levels of rat Nlrp3, Hmgb1, IL‐1β , and IL‐17a were evaluated by quantitative real‐time polymerase chain reaction. Histopathological examination of the small intestinal tissues of the studied rats was performed. There was a significant upregulation of the rat Nlrp3 , IL‐1β, IL‐17a mRNA expression ( p < 0.001 for the three parameters), and Hmgb1 ( p < 0.05) in the untreated IBD group compared to the normal control group. In the MSC‐treated group, IL‐1β, IL‐17a , and rat Nlrp3 mRNA expression significantly decreased compared to both the untreated IBD group and PBS group ( p < 0.05 for all). hUCB‐MSCs ameliorated IBD in rats by downregulating the pro‐inflammatory cytokines ( IL‐1β and IL‐17a ) and other inflammatory mediators such as Hmgb1 and rat Nlrp3 .
科研通智能强力驱动
Strongly Powered by AbleSci AI