摘要
目的:研究表没食子儿茶素-3-没食子酸酯(EGCG)的抗肝纤维化作用及其机制.方法:运用腹腔注射CCl4构建大鼠肝纤维化模型,观察EGCG对大鼠肝纤维化的影响.运用HE染色、Massion三色染色检测肝纤维化的变化;生化检测血清丙氨酸转移酶(ALT)及天冬氨酸转移酶(AST);同时检测肝组织的羟脯氨酸、还原型谷胱甘肽(GSH)和硫代巴比妥酸反应底物(TBARS)含量.免疫组织化学法观察α-平滑肌肌动蛋白(α-SMA)的表达;分别运用RT-PCR和Western blot法检测转化生长因子β1(TGF-β1)及结缔组织生长因子(CTGF)mRNA和蛋白质表达.结果:EGCG对CCl4诱导的大鼠肝纤维化程度具有显著的抑制作用.EGCG对肝细胞具有显著的保护作用,与纤维化模型组比较,EGCG干预组血清ALT、AST水平降低(138.4±45.8vs234.6±63.2,96.4±20.5vs186.2±36.6,均P<0.05).EGCG显著抑制肝组织α-SMA的表达.EGCG通过抑制TBARS的形成和提高GSH含量,显著改善CCl4诱导的肝纤维化大鼠肝脏的氧化状态.同时EGCG显著抑制肝组织TGF-β1及CTGF的mRNA和蛋白质的表达(均P<0.05).结论:EGCG能够显著抑制肝纤维化的进展,其机制与EGCG改善大鼠肝脏的氧化状态及抑制TGF-β1和CTGF的表达有关.
AIM： To examine the protective effects of epigallocatechin-3-gallate （EGCG） on CC14- induced hepatic fibrosis.
METHODS： A rat model of CCl4-induced hepatic fibrosis was established to assess the effect of EGCG on the treatment for fibrosis. Liver fibrosis of the rats was evaluated by two histological methods： HE staining and Masson＇s trichrome staining. Activities of serum ALT and AST were checked with automated biochemistry analyzer. The levels of liver tissue hydroxyproline, glutathione （GSH） and thiobarbituratic acid reactive substances （TBARS） were also determined. The expression of α-SMA in hepatic tissue was detected by immunohistochemistry. The mRNA and protein levels of TGF-β1 and CTGF expression were detected by RT-PCR and Western blot analysis.
RESULTS： Histological and hepatic hydroxyproline examination revealed that EGCG significantly arrested progression of hepatic fibrosis. EGCG caused significant amelioration of liver injury, and reduced activities of serum ALT and AST （138.4 ± 45.8 vs 234.6 ± 63.2, 96.4 ± 20.5 vs 186.2 ± 36.6, both P 〈 0.05）. Redox state was improved in CCl4-induced hepatic fibrosis through treatment with EGCG, by suppressing the TBARS formation and increasing the level of GSH. Moreover, EGCG markedly reduced both mRNA and protein expression of TGF-β1 and CTGF in the liver tissue （P 〈 0.05）.
CONCLUSION： EGCG significantly arrested progression of hepatic fibrosis. The underlying mechanism was associated with changes in the redox state and markedly decreased expression of TGF and CTGF in liver tissue.
出处
《世界华人消化杂志》
CAS
北大核心
2008年第34期3828-3834,共7页
World Chinese Journal of Digestology
