Hepatoprotective Effect of Pinoresinol on Carbon Tetrachloride-Induced Hepatic Damage in Mice
Hepatoprotective Effect of Pinoresinol on Carbon Tetrachloride-Induced Hepatic Damage in Mice
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DOI：
10.1254/jphs.09234fp
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发表时间：
2010-01-01
影响因子：
3.5
通讯作者：
Lee, Sun-Mee
中科院分区：
文献类型：
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作者：
Kim, Hyo-Yeon;Kim, Joon-Ki;Lee, Sun-Mee
众所周知，连翘具有利尿、抗菌和抗炎活性。本研究探讨了松脂醇对四氯化碳(CCl4)所致小鼠肝损伤的保护作用。在注射四氯化碳(20亩L/kg)前30min和注射后2 h，分别给予赋形剂或松脂醇(25、50、100、200 mg/kg)处理。在赋形剂处理组，CCl4注射后24 h，血清转氨酶活性显著升高，而松脂醇各剂量组的升高均被松脂醇所减弱。经CCl4处理后，肝组织谷胱甘肽含量明显降低，脂质过氧化反应增强。50 mg/kg和100 mg/kg松脂醇可减轻上述变化。注射CCl_4后，炎性介质肿瘤坏死因子-α、诱导型一氧化氮合酶和环氧合酶-2的蛋白和mRNA表达水平显著升高，松脂醇可减弱这种上调。松脂醇抑制活化蛋白1(AP-1)的核因子-kappaB(NF-kappa B)核转位和c-jun的磷酸化。我们的结果表明，松脂醇可以减轻CCl4诱导的急性肝损伤，这种保护作用可能是通过抑制核因子-kappaB和AP-1而发挥抗氧化活性和下调炎症介质的作用。
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 mu l/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-alpha, 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-kappa B (NF-kappa B) 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-kappa B and AP-1.