Effect of Astragalus polysaccharide on pancreatic cell mass in type 1 diabetic mice.
- Author:
Ru-Jiang LI
1
;
Shu-Dong QIU
;
Hong-Xia CHEN
;
Hong TIAN
;
Guo-Qiang LIU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; drug effects; Astragalus membranaceus; chemistry; Carrier Proteins; metabolism; Diabetes Mellitus, Experimental; chemically induced; metabolism; pathology; Diabetes Mellitus, Type 1; chemically induced; metabolism; pathology; Enzyme-Linked Immunosorbent Assay; Insulin-Secreting Cells; drug effects; metabolism; pathology; Interferon-gamma; metabolism; Interleukin-4; metabolism; Islets of Langerhans; drug effects; metabolism; pathology; Lithostathine; biosynthesis; genetics; Male; Mice; Mice, Inbred C57BL; Plants, Medicinal; chemistry; Polysaccharides; isolation & purification; pharmacology; RNA, Messenger; biosynthesis; genetics; Reverse Transcriptase Polymerase Chain Reaction; Streptozocin; Transcription Factors
- From: China Journal of Chinese Materia Medica 2007;32(20):2169-2173
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effect of Astragalus polysaccharide (APS) on pancreatic beta cell mass in type 1 diabetic mice.
METHODDiabetic 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.
RESULTAttenuated 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.
CONCLUSIONAPS can upregulate pancreatic beta cell mass in type 1 diabetic mice, strongly associated with improved autoimmunity.
