[Protective effect of Angelica sinensis polysaccharide against liver injury induced by D-galactose in aging mice and its mechanisms].
OBJECTIVE
To investigate the protective effect of Angelica sinensis polysaccharide (ASP) against liver injury induced by D-galactose in aging mice and its mechanisms.


METHODS
Male C57BL/6J were randomly divided into three groups with 10 mice in each group. In the D-galactose model group, the mice were subcutaneously injected with D-galactose (120 mg/kg) qd×42; in the ASP+D-galactose group, from the 8th day of the establishment of D-galactose model, the mice were subcutaneously injected with ASP (120 mg/kg) qd×35. In the normal control group, the mice were subcutaneously injected with isotonic saline of the same volume at the same time point. On the 2nd day after the injection was finished, the ocular blood was collected to prepare serum and measure the content of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and total bilirubin (TBil). The liver tissue homogenate was prepared to measure the content of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), and advanced glycation end products (AGEs). A paraffin section of liver tissue was prepared; HE staining was performed to observe the pathomorphological changes of the liver, periodic acid-Schiff staining (PAS) was used to observe the changes in glycogen in the liver, and a transmission electron microscope was used to observe the hepatocyte ultrastructure.


RESULTS
The D-galactose model group had increased content of ALT, AST, and TBil, reduced activities of SOD and GSH-Px, an increased content of MDA, and severe liver injuries; the hepatocytes showed degenerative changes, the amount of glycogen in the liver decreased, and the accumulation of AGEs increased. The ASP+D-galactose group had reduced content of ALT, AST, and TBil, increased activities of SOD and GSH-Px, and reduced content of MDA and AGEs; the amount of glycogen in the liver increased, and liver injury and hepatocyte injury were alleviated.


CONCLUSIONS
ASP can antagonize the liver injury induced by D-galactose in aging mice, and its mechanism may be related to the inhibition of oxidative stress.
Laboratory of Stem Cells and Tissue Engineering, Department of Histology and Embryology, Chongqing Medical University, Chongqing 400016, China.
J Y
JY
Xia
Y L
YL
Fan
D Y
DY
Jia
M S
MS
Zhang
Y Y
YY
Zhang
J
J
Li
P W
PW
Jing
L
L
Wang
Y P
YP
Wang
D000410:Alanine Transaminase / Q000378:metabolism; D029971:Angelica sinensis / Q000737:chemistry*; D000818:Animals; D001219:Aspartate Aminotransferases / Q000378:metabolism; D056486:Chemical and Drug Induced Liver Injury / Q000188:drug therapy*; D004365:Drugs, Chinese Herbal / Q000008:administration & dosage*; D005690:Galactose; D005979:Glutathione Peroxidase; D022781:Hepatocytes; D008099:Liver; D008297:Male; D008315:Malondialdehyde; D051379:Mice; D008810:Mice, Inbred C57BL; D018384:Oxidative Stress; D011134:Polysaccharides / Q000008:administration & dosage*; D020011:Protective Agents / Q000008:administration & dosage* / Q000494:pharmacology; D013482:Superoxide Dismutase / Q000378:metabolism
D004365:Drugs, Chinese Herbal; D011134:Polysaccharides; D020011:Protective Agents; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D005690:Galactose