TY - JOUR
T1 - Effects of 1-O-hexyl-2,3,5-trimethylhydroquinone on carbon tetrachloride-induced hepatic cirrhosis in rats
AU - An, Jun
AU - Feng, Guo Gang
AU - Huang, Lei
AU - Kurokawa, Tsuyoshi
AU - Nonami, Toshiaki
AU - Koide, Tatsuro
AU - Kondo, Fumio
AU - Komatsu, Toru
AU - Tsunekawa, Koji
AU - Fujiwara, Yoshihiro
AU - Goto, Hidemi
AU - Nishikawa, Hiroshi
AU - Miki, Tokutaro
AU - Sugiyama, Satoru
AU - Ishikawa, Naohisa
PY - 2010/6
Y1 - 2010/6
N2 - 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 (CCl4)-induced cirrhosis. Methods: Rats were treated with hypodermic injections of CCl4 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 CCl4 group, the lesions being reduced in the CCl4 HTHQ group. Increases in liver tissue hydroxyproline and α1(I) collagen, α-smooth muscle actin and iNOS induced by CCl4, were also markedly diminished by HTHQ. Furthermore, both HTHQ and vitamin E attenuated interleukin-1β-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.
AB - 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 (CCl4)-induced cirrhosis. Methods: Rats were treated with hypodermic injections of CCl4 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 CCl4 group, the lesions being reduced in the CCl4 HTHQ group. Increases in liver tissue hydroxyproline and α1(I) collagen, α-smooth muscle actin and iNOS induced by CCl4, were also markedly diminished by HTHQ. Furthermore, both HTHQ and vitamin E attenuated interleukin-1β-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.
UR - http://www.scopus.com/inward/record.url?scp=77954359136&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=77954359136&partnerID=8YFLogxK
U2 - 10.1111/j.1872-034X.2010.00638.x
DO - 10.1111/j.1872-034X.2010.00638.x
M3 - Article
AN - SCOPUS:77954359136
SN - 1386-6346
VL - 40
SP - 613
EP - 621
JO - Hepatology Research
JF - Hepatology Research
IS - 6
ER -
