College of Pharmacy, Pusan National University, Busan, 609-735, Korea.
Arch Pharm Res. 2013 May;36(5):626-33. doi: 10.1007/s12272-013-0050-5. Epub 2013 Mar 15.
Acute hepatic inflammation is regarded as a hallmark of early stage fibrosis, which can progress to extensive fibrosis and cirrhosis. Sinapic acid is a phenylpropanoid compound that is abundant in cereals, nuts, oil seeds, and berries and has been reported to exhibit a wide range of pharmacological properties. In this study, we investigated the anti-inflammatory effect of sinapic acid in carbon tetrachloride (CCl4)-induced acute hepatic injury in rats. Sinapic acid was administered orally (10 or 20 mg/kg) to rats at 30 min and 16 h before CCl4 intoxication. Sinapic acid treatment of rats reduced CCl4-induced abnormalities in liver histology, serum alanine transaminase and aspartate transaminase activities, and liver malondialdehyde levels. In addition, sinapic acid treatment significantly attenuated the CCl4-induced production of inflammatory mediators, including tumor necrosis factor-alpha and interleukin-1β mRNA levels, and increased the expression of nuclear factor-kappa B (NF-κB p65). Sinapic acid exhibited strong free radical scavenging activity in vitro. Thus, sinapic acid protected the rat liver from CCl4-induced inflammation, most likely by acting as a free radical scavenger and modulator of NF-κB p65 activation and proinflammatory cytokine expression. Sinapic acid may thus have potential as a therapeutic agent for suppressing hepatic inflammation.
急性肝炎症被视为早期纤维化的标志，它可进展为广泛纤维化和肝硬化。芥子酸是一种苯丙烷类化合物，在谷物、坚果、油籽和浆果中含量丰富，据报道具有广泛的药理作用。在本研究中，我们研究了芥子酸对 CCl4 诱导的大鼠急性肝损伤的抗炎作用。在 CCl4 中毒前 30 分钟和 16 小时，通过口服给予大鼠芥子酸（10 或 20mg/kg）。芥子酸处理大鼠降低了 CCl4 引起的肝组织学、血清丙氨酸转氨酶和天冬氨酸转氨酶活性以及肝丙二醛水平的异常。此外，芥子酸处理显著减弱了 CCl4 诱导的炎症介质的产生，包括肿瘤坏死因子-α和白细胞介素-1βmRNA 水平的增加，并增加了核因子-κB（NF-κB p65）的表达。芥子酸在体外表现出很强的自由基清除活性。因此，芥子酸通过作为自由基清除剂和 NF-κB p65 激活和促炎细胞因子表达的调节剂来保护大鼠肝脏免受 CCl4 诱导的炎症，可能具有作为抑制肝炎症的治疗剂的潜力。
