Study on Protective Effects of Salidrosides on Pancreaticβ-Cell Survival
10.14148/j.issn.1672-0482.2016.0456
- VernacularTitle:红景天苷对胰岛β细胞保护作用研究及机制探讨
- Author:
Ie Lin-j JU
1
;
Xiao-Hua WEN
;
Luan SHU
Author Information
1. 安徽中医药大学药学院
- Keywords:
salidroside;
diabetes;
pancreatic β-cell;
proliferation;
apoptosis
- From:
Journal of Nanjing University of Traditional Chinese Medicine
2016;32(5):456-460
- CountryChina
- Language:Chinese
-
Abstract:
ABSTRACT:OBJECTIVE To investigate the hypoglycemic action and β-cell protective effect of salidroside in streptozotocin (STZ) induced diabetic mice and cultured mouse islets.METHODS C57BL∕6J mice were injected with a single dose of 1 50 mg∕kg freshly prepared STZ with citrate buffer as control.The salidroside intervention with a dosage of 100 mg∕kg∕d was ini-tiated on the 8th day after STZ injection and conducted for 30 d.Fasting blood glucose levels were measured every five days. After 30 d treatment,the oral glucose tolerance test(OGTT)was performed,and blood samples were collected to detect plas-ma insulin concentrations.The isolated mouse islets were cultured with salidroside(50 μmol∕L) or DMSO for 3 d.Ki67 stai-ning and TUNEL assay were performed to investigate the effects of salidroside on β-cell proliferation and apoptosis.Mean-while,the mRNA levels of insulin,Pdx-1,GLP-1R and IL-1βin islets were detected by RT-PCR.RESULTS Compared with the STZ group,salidroside displayed significantly hypoglycemic effects,together with increased plasma insulin contents as well as improved OGTT.The Ki67 staining in cultured islets showed the proliferation ofβ-cell was remarkably increased by salidro-side,while the β-cell apoptosis induced by high glucose was strongly inhibited by salidroside.Moreover,the mRNA levels of insulin,Pdx-1 and GLP-1R were up-regulated by salidroside significantly.However,the mRNA level of IL-1βwhich is a cyto-kine involved inβ-cell apoptosis was down-regulated by salidroside.CONCLUSION The present study demonstrates that sali-droside can ameliorate the hyperglycemia in STZ diabetic mice by protecting β-cell survival with increased β-cell proliferation and decreasedβ-cell apoptosis.
