胰岛炎
链脲佐菌素
内分泌学
内科学
下调和上调
细胞凋亡
胰腺
β细胞
细胞因子
小岛
化学
胰岛素
生物
糖尿病
医学
生物化学
基因
作者
Rujiang Li,Shu-Dong Qiu,Hongxia Chen,Hong Tian,Guoqiang Liu
出处
期刊:PubMed
日期:2007-10-01
卷期号:32 (20): 2169-73
被引量:7
摘要
To study the effect of Astragalus polysaccharide (APS) on pancreatic beta cell mass in type 1 diabetic mice.Diabetic mice induced by multiple low dose streptozotocin (MLD-STZ) were administered either APS (100, 200, 400 mg x kg(-1) body weight) or saline intraperitoneally daily, and sacrificed after 15 or 30 days of treatment. Streptavidin-peroxidase immunohistochemical method with counterstain was performed to determine the effect of APS on insulitis. Indirect double immunofluorescence for Insulin/Ki67 (counterstained by Hoechst33258) and Insulin/Cleaved caspase-3 was used to evaluate pancreatic cell (besides beta cell) proliferation, beta cell neogenesis, beta cell apoptosis and beta cell mass. Semi-quantitative RT-PCR was utilized to characterize pancreatic regenerating protein 1 mRNA levels, and ELISA method was performed to measure the levels of cytokine IFN-gamma and IL-4 secreted by splenocytes.Attenuated insulitis, upregulated beta cell mass, increased number of neogenetic pancreas islets, decreased number of apoptosis beta cells and downregulation of Th1/Th2 cytokine ratio were significantly time-and dose-dependent on APS treatment, when compared to saline controls. However, no significant differences of the number of pancreatic proliferative cells or replicative cells and pancreatic regenerating protein 1 mRNA levels were demonstrated between APS (APS100, APS200 and APS400) and saline vehicle group on day 15 and 30 with APS treatment.APS can upregulate pancreatic beta cell mass in type 1 diabetic mice, strongly associated with improved autoimmunity.
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