Kim Tae-Won, Lee Dong-Ryung, Choi Bong-Keun, Kang Hwan-Kyu, Jung Ju-Young, Lim Seol-Wa, Yang Seung Hwan, Suh Joo-Won
College of Veterinary Medicine & Institute of Veterinary Science, Chungnam National University, Yusung-gu, Daejeon, 305-764, South Korea.
NutraPham Tech, Yongin, Gyeonggi, 449-728, South Korea.
Food Chem Toxicol. 2016 May;91:91-9. doi: 10.1016/j.fct.2016.03.004. Epub 2016 Mar 12.
In the present study, we explore the protective effects of Citrus aurantium L. extract (CAE) against acute and chronic CCl4-induced hepatotoxicity. The quantitative analysis of CAE was performed using HPLC-UV to determine the nobiletin content was approximately 27%. For the acute model, the male ICR mice were orally treated with water, silymarin (positive control, 200 mg/kg) and CAE (50 and 200 mg/kg) for 3 days prior to CCl4 (1 mL/kg, 50% v/v in olive oil) IP injection. For the chronic model (n = 6/group), the mice were treated with each treatment for 28 consecutive days and CCl4 (1 mL/kg, 20%) was injected twice a week. In both the acute and chronic models, the CCl4 alone treated group showed histopathologic alterations with a significantly increase in serum hepatic enzyme levels together with a disrupted anti-oxidative status. In contrast, the CAE treatments restored pathologic alterations and recovered the oxidative status by enhancing antioxidant enzymes and reducing lipid peroxidation levels. Furthermore, CAE enhanced nuclear factor E2-related factor 2 (Nrf2) and its related cytoprotective signals, including NAD(P)H quinone oxidoreductase 1, UDP-glucuronosyltransferase, and γ-glutamylcysteine synthetase. Taken together, the present study demonstrates that CAE exerts a protective effect against CCl4-induced hepatotoxicity with its anti-oxidant, anti-inflammatory, and anti-apoptotic activity.
在本研究中,我们探讨了枳实提取物(CAE)对急性和慢性四氯化碳诱导的肝毒性的保护作用。使用高效液相色谱-紫外检测法对CAE进行定量分析,以确定川陈皮素含量约为27%。对于急性模型,雄性ICR小鼠在腹腔注射四氯化碳(溶于橄榄油,1 mL/kg,50% v/v)前3天,分别口服给予水、水飞蓟宾(阳性对照,200 mg/kg)和CAE(50和200 mg/kg)。对于慢性模型(每组n = 6),小鼠连续28天接受每种处理,每周两次注射四氯化碳(1 mL/kg,20%)。在急性和慢性模型中,单独给予四氯化碳处理的组均显示出组织病理学改变,血清肝酶水平显著升高,同时抗氧化状态受到破坏。相比之下,CAE处理可恢复病理改变,并通过增强抗氧化酶和降低脂质过氧化水平来恢复氧化状态。此外,CAE增强了核因子E2相关因子2(Nrf2)及其相关的细胞保护信号,包括NAD(P)H醌氧化还原酶1、尿苷二磷酸葡萄糖醛酸转移酶和γ-谷氨酰半胱氨酸合成酶。综上所述,本研究表明,CAE通过其抗氧化、抗炎和抗凋亡活性对四氯化碳诱导的肝毒性发挥保护作用。