Article

Evaluation of antidiabetic activity of polysaccharide isolated from Phellinus linteus in non-obese diabetic mouse.

Korea Research Institute of Bioscience and Biotechnology, Chungbuk, Republic of Korea.
International immunopharmacology (impact factor: 2.21). 10/2009; 10(1):72-8. DOI:10.1016/j.intimp.2009.09.024 pp.72-8
Source: PubMed

ABSTRACT Polysaccharide (PLP) isolated from Phellinus linteus inhibits tumor growth and metastasis by enhancing immune functions of macrophages, dendritic cells, NK cells, T cells, and B cells. Here, we report that PLP can inhibit the development of autoimmune diabetes in non-obese diabetic (NOD) mice. Although 80% of the NOD mice had developed diabetes by 24 weeks of age, none of the PLP-treated NOD mice developed diabetes. The mean blood glucose levels were 110mg/dl in PLP-treated mice and 499mg/dl in control NOD mice. Histological examination of the pancreatic islets revealed that most of the islets isolated from PLP-treated mice were less infiltrated with lymphocytes compared with those of control mice. Spleen cells from diabetic NOD mice could adaptively transfer diabetes into NOD/SCID mice, but those from PLP-treated NOD mice showed delayed transfer of diabetes. PLP inhibited the expression of inflammatory cytokines, including IFN-gamma, IL-2, and TNF-alpha by Th1 cells and macrophages, but up-regulated IL-4 expression by Th2 cells in NOD mice. PLP did not prevent streptozotocin-induced diabetic development in ICR mice. Taken together, these results suggest that PLP inhibits the development of autoimmune diabetes by regulating cytokine expression.

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Keywords

autoimmune diabetes
 
control mice
 
control NOD mice
 
diabetes
 
diabetic NOD mice
 
Histological examination
 
immune functions
 
inflammatory cytokines
 
mean blood glucose levels
 
non-obese diabetic
 
pancreatic islets
 
Phellinus linteus inhibits tumor growth
 
PLP inhibits
 
PLP-treated mice
 
PLP-treated NOD mice
 
regulating cytokine expression
 
streptozotocin-induced diabetic development
 
Th1 cells
 
Th2 cells
 
up-regulated IL-4 expression