Effects of Rehmannia glutinosa oligosaccharides on proliferation of HepG2 and insulin resistance.
- Author:
Li-min GUO
1
;
Ru-xue ZHANG
;
Zheng-ping JIA
;
Mao-xing LI
;
Juan WANG
;
Qiang YIN
Author Information
- Publication Type:Journal Article
- MeSH: Carcinoma, Hepatocellular; metabolism; pathology; Cell Line, Tumor; Cell Proliferation; drug effects; Cell Survival; drug effects; Dose-Response Relationship, Drug; Drug Resistance, Neoplasm; Glucose; metabolism; pharmacology; Humans; Hypoglycemic Agents; isolation & purification; pharmacology; Insulin; pharmacology; Insulin Resistance; Liver Neoplasms; metabolism; pathology; Oligosaccharides; isolation & purification; pharmacology; Plants, Medicinal; chemistry; Rehmannia; chemistry
- From: China Journal of Chinese Materia Medica 2007;32(13):1328-1332
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of Rehmannia glutinosa oligosaccharides (ROS) on the proliferation of HepG2 and insulin resistance.
METHODThe HepG2 cells were divided into control group, rosiglitazone (3.4 mg x L(-1)) treated group and ROS (0.1-30 mg x L(-1)) treated group. The proliferation of HepG2 was detected by MTT method. Insulin resistant HepG2 cells model was induced by high concentration of insulin, then the effects of ROS on glucose consumption in insulin resistant HepG2 cells were investigated.
RESULTIn the middle glucose culture medium, the absorbance at 570 nm of HepG2 was increased by high concentration of ROS, and decreased by low concentration of ROS by using MTT method, a concentration-dependent manner. ROS increased glucose consumption in HepG2 cells, and showed a better effect at the dose of 10 mg x L(-1). ROS promoted the glucose consumption in insulin resistance of HepG2 cells, improved the sensitivity of insulin resistance of HepG2 cells to insulin.
CONCLUSIONHigh concentration of ROS can promote the proliferation of HepG2, and however low concentration of ROS inhibits the proliferation of HepG2. ROS can significantly improve insulin resistance of HepG2 cells induced by high insulin.
