Effects of 1-O-hexyl-2,3,5-trimethylhydroquinone on carbon tetrachloride-induced hepatic cirrhosis in rats

Autor: Toshiaki Nonami, Yoshihiro Fujiwara, Hidemi Goto, Koji Tsunekawa, Tsuyoshi Kurokawa, Tatsuro Koide, Fumio Kondo, Toru Komatsu, Jun An, Naohisa Ishikawa, Guo-Gang Feng, Satoru Sugiyama, Tokutaro Miki, Hiroshi Nishikawa, Lei Huang
Rok vydání: 2010
Předmět:
Zdroj: Hepatology Research. 40:613-621
ISSN: 1386-6346
DOI: 10.1111/j.1872-034x.2010.00638.x
Popis: AIM The present study was undertaken to evaluate the effects of 1-O-hexyl-2,3,5-trimethylhydroquinone (HTHQ), a synthesized vitamin E derivative, on carbon tetrachloride (CCl(4))-induced cirrhosis. METHODS Rats were treated with hypodermic injections of CCl(4) twice a week to induce the hepatic cirrhosis, and given drinking water containing HTHQ or solvent. Primary cultures of rat hepatocytes were performed to evaluate the effects of HTHQ on the expression of inducible nitric oxide synthase (iNOS). RESULTS Masson's staining of rat livers showed fibrosis around pseudo-lobules in the CCl(4) group, the lesions being reduced in the CCl(4) HTHQ group. Increases in liver tissue hydroxyproline and alpha(1)(I) collagen, alpha-smooth muscle actin and iNOS induced by CCl(4), were also markedly diminished by HTHQ. Furthermore, both HTHQ and vitamin E attenuated interleukin-1beta-induced iNOS protein expression in cultured hepatocytes, the potency of HTHQ being 10-times higher than that of vitamin E. CONCLUSION HTHQ may inhibit development of hepatic cirrhosis in rats, more potently than vitamin E, by inhibiting the iNOS expression in hepatocytes. Because vitamin E has a radical scavenging action, roles of NO and peroxynitrite will be discussed in the effects of HTHQ on the fibrosis.
Databáze: OpenAIRE
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