Hepatoprotective Effect of Pinoresinol on Carbon Tetrachloride–Induced Hepatic Damage in Mice

Journal of Pharmacological Sciences

Seung-Ho Lee²  Sun-Mee Lee³  Dong Chun Kim²  Yeong Shik Kim¹  Woo-Yong Oh³  Jun-Ho Choi³  Joon-Ki Kim³  Sam Sik Kang¹  Hee Sang Lee²  Hyo-Yeon Kim³  Joo-Yeon Jung³ 

[1] College of Pharmacy, Seoul National University, Korea;College of Pharmacy, Yeungnam University, Korea;School of Pharmacy, Sungkyunkwan University, Korea

关键词: carbon tetrachloride;    hepatoprotective activity;    inflammation;    oxidative stress;    pinoresinol;   

DOI  :  10.1254/jphs.09234FP

学科分类：药学

来源: Nihon Yakuri Gakkai Henshuubu / Japanese Pharmacological Society

【 摘 要 】

References(35)Cited-By(36)Forsythiae Fructus is known to have diuretic, anti-bacterial, and anti-inflammatory activities. This study examined the hepatoprotective effects of pinoresinol, a lignan isolated from Forsythiae Fructus, against carbon tetrachloride (CCl4)–induced liver injury. Mice were treated intraperitoneally with vehicle or pinoresinol (25, 50, 100, and 200 mg/kg) 30 min before and 2 h after CCl4 (20 μl/kg) injection. In the vehicle-treated CCl4 group, serum aminotransferase activities were significantly increased 24 h after CCl4 injection, and these increases were attenuated by pinoresinol at all doses. Hepatic glutathione contents were significantly decreased and lipid peroxidation was increased after CCl4 treatment. These changes were attenuated by 50 and 100 mg/kg of pinoresinol. The levels of protein and mRNA expression of inflammatory mediators, including tumor necrosis factor-α, inducible nitric oxide synthase, and cyclooxygenase-2, were significantly increased after CCl4 injection; and these increases were attenuated by pinoresinol. Nuclear translocation of nuclear factor-κB (NF-κB) and phosphorylation of c-Jun, one of the components of activating protein 1 (AP-1), were inhibited by pinoresinol. Our results suggest that pinoresinol ameliorates CCl4-induced acute liver injury, and this protection is likely due to anti-oxidative activity and down-regulation of inflammatory mediators through inhibition of NF-κB and AP-1.

【 授权许可】

Unknown