Antioxidative and hypolipidemic effects of diosgenin, a steroidal saponin of yam (Dioscorea spp.), on high-cholesterol fed rats.
Diosgenin (a steroidal saponin of yam) has long been used as a raw material for the industrial production of steroid drugs, and reported to have a hypocholesterolemic effect by suppressing cholesterol absorption and increasing cholesterol secretion. Oxidative stress has been suggested as a main risk factor in the development of atherosclerosis. The aim of this study is to investigate the possible hypolipidemic and antioxidative effect of diosgenin on rats fed with a high-cholesterol diet supplemented with either 0.1% or 0.5% diosgenin for 6 weeks. We measured the lipid profile in the plasma and liver, lipid peroxidation and antioxidative enzyme activities in the plasma, erythrocyte and gene expression of antioxidative enzymes in the liver, and the oxidative DNA damage in lymphocytes. Diosgenin showed a decrease in the plasma and hepatic total cholesterol levels, but increased the plasma high-density lipoprotein (HDL) cholesterol level. Erythrocyte TBARS and lymphocyte DNA damage measured by the comet assay were decreased in the diosgenin supplemented group. Furthermore, diosgenin feeding enhanced the resistance to lymphocyte DNA damage caused by an oxidant challenge with H(2)O(2). The antioxidative enzyme activities were also affected by diosgenin supplementation. Total superoxide dismutase (SOD) in the plasma and liver, glutathione peroxidase (GSH-Px) in erythrocytes, and catalase (CAT) in erythrocytes and liver were significantly increased in the 0.5% diosgenin group. The expression of antioxidative enzymes was up-regulated by diosgenin, the expression of GSH-Px being the highest in the 0.5% diosgenin group. These results suggest that diosgenin could be a very useful compound to control hypercholesterolemia by both improving the lipid profile and modulating oxidative stress.
Son
In Suk
IS
Department of Food Science and Nutrition, Andong National University, Andong, Korea.
Kim
Ji Hyun
JH
Sohn
Ho Yong
HY
Son
Kun Ho
KH
Kim
Jong-Sang
JS
Kwon
Chong-Suk
CS
D000818:Animals; D000924:Anticholesteremic Agents / Q000494:pharmacology; D000975:Antioxidants / Q000494:pharmacology*; D002374:Catalase / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D004249:DNA Damage / Q000187:drug effects; D004036:Diet, Atherogenic; D027742:Dioscorea / Q000737:chemistry*; D004144:Diosgenin / Q000494:pharmacology*; D004789:Enzyme Activation; D004912:Erythrocytes / Q000187:drug effects / Q000201:enzymology; D005979:Glutathione Peroxidase / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000494:pharmacology; D006937:Hypercholesterolemia / Q000188:drug therapy; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects / Q000201:enzymology*; D008214:Lymphocytes / Q000187:drug effects / Q000201:enzymology; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism
D000924:Anticholesteremic Agents; D000975:Antioxidants; D002784:Cholesterol; D006861:Hydrogen Peroxide; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D004144:Diosgenin