Increased galectin-1 expression in muscle of Astragalus polysaccharide-treated Type 1 diabetic mice

In order to investigate the immunopharmacological function of Astragalus polysaccharide (APS) in Type 1 diabetes mellitus (T1DM), multiple low-dose streptozotocin-induced diabetic mice and normal mice were administered either APS or saline intraperitoneally once daily. The changes in galectin-1 expr...

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Bibliographic Details
Published inJournal of natural medicines Vol. 65; no. 3-4; pp. 500 - 507
Main Authors Zhou, Xingjian, Xu, Yancheng, Yang, Guoming, Li, Fang
Format Journal Article
LanguageEnglish
Published Japan Springer Japan 01.07.2011
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Summary:In order to investigate the immunopharmacological function of Astragalus polysaccharide (APS) in Type 1 diabetes mellitus (T1DM), multiple low-dose streptozotocin-induced diabetic mice and normal mice were administered either APS or saline intraperitoneally once daily. The changes in galectin-1 expression in different organs of the mice were detected by ELISA, Real-time fluorescence quantitative RT-PCR and Western blot. The percentages of apoptotic CD8 + T cells from spleens of APS-treated diabetic mice were measured by flow cytometry. We found that the expression of galectin-1 was increased in serum of APS-treated diabetic mice compared to the non-treated diabetic mice (* p  < 0.05). Increased galectin-1 was mainly expressed in the muscle of APS-treated mice. In vitro, APS up-regulated the expression of galectin-1 in muscle cells in a dose-dependent manner. The percentage of apoptotic CD8 + T cells in spleens of APS-treated mice was positively correlated with the concentration of APS treatment, and the blocking of galectin-1 in vivo by specific antibody reduced the percentage of apoptotic CD8 + T cells in APS-treated mice. Our findings indicated that APS could up-regulate the expression of galectin-1 in muscle of T1DM mice, resulting in the apoptosis of CD8 + T cells. This may be an important mechanism by which APS protects β cells of the pancreatic islets from apoptosis induced by CD8 + T cells in T1DM in vivo.
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ISSN:1340-3443
1861-0293
1861-0293
DOI:10.1007/s11418-011-0527-9