Protective effect of picroliv against hydrazine-induced hyperlipidemia and hepatic steatosis in rats.
The protective effect of picroliv (PIC) obtained from Picrorhiza kurroa (family: Scrophulariaceae) against hydrazine (Hz)-induced hyperlipidemia was evaluated in rats. Hz administration (50 mg/kg, i.p.) caused an increase in triglyceride (TG), cholesterol (CHO), free fatty acids (FFA), and total lipids (TL) in both the plasma and liver tissue of rats accompanied by a fall in phospholipids (PL) in the liver tissue 24 h after its administration, indicating its hyperlipidemic property. The above abnormality was prevented by simultaneous treatment of PIC (50 mg/kg, p.o.) with Hz. Hz treatment also caused an increase in the mobility of TG and TL from adipose tissue, and these results indicate that Hz administration could cause hepatic steatosis by nonhepatocellular factors (such as mobilization of depot fats). This effect was also prevented by simultaneous treatment of PIC with Hz. PIC-alone treatment, however, did not produce any change in the status of all the lipid parameters evaluated in plasma, liver, and adipose tissues. These results indicate that increased mobilization of depot fats from adipose tissue may contribute to the development of hepatic steatosis in addition to decreased lipoprotein secretion, increased hepatic TG biosynthesis, and increased hepatic uptake of FFA. These have been reported as the mechanism responsible for the development of Hz-induced hepatic steatosis. PIC prevents Hz-induced hyperlipidemia, hepatic steatosis, and mobilization of lipids from depot fats, but the mechanism behind the protective effect of PIC remains to be elucidated.
Vivekanandan
P
P
Department of Pharmacology and Environmental Toxicology, Dr. A. L. M. Postgraduate Institute of Basic Medical Sciences, University of Madras, Chennai, India.
Gobianand
K
K
Priya
S
S
Vijayalakshmi
P
P
Karthikeyan
S
S
D000273:Adipose Tissue / Q000187:drug effects* / Q000378:metabolism; D000818:Animals; D002784:Cholesterol / Q000097:blood / Q000378:metabolism; D002934:Cinnamates / Q000494:pharmacology* / Q000627:therapeutic use; D004195:Disease Models, Animal; D005230:Fatty Acids, Nonesterified / Q000097:blood / Q000378:metabolism; D005234:Fatty Liver / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D006027:Glycosides / Q000494:pharmacology* / Q000627:therapeutic use; D006834:Hydrazines; D006949:Hyperlipidemias / Q000139:chemically induced / Q000150:complications / Q000378:metabolism / Q000517:prevention & control*; D000960:Hypolipidemic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D050356:Lipid Metabolism / Q000187:drug effects*; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D010743:Phospholipids / Q000097:blood / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D014280:Triglycerides / Q000097:blood / Q000378:metabolism; D014641:Vanillic Acid / Q000494:pharmacology* / Q000627:therapeutic use
D002934:Cinnamates; D005230:Fatty Acids, Nonesterified; D006027:Glycosides; D006834:Hydrazines; D000960:Hypolipidemic Agents; D010743:Phospholipids; D014280:Triglycerides; C057463:kutkin; C029424:hydrazine; D002784:Cholesterol; D014641:Vanillic Acid