Antioxidative effects of Alisma orientale extract in palmitate-induced cellular injury
Antioxidative effects of Alisma orientale extract in palmitate-induced cellular injury
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DOI：
10.3109/13880209.2012.673629
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发表时间：
2012-10-01
影响因子：
3.8
通讯作者：
Seo, Han Geuk
中科院分区：
文献类型：
--
作者：
Han, Chang Woo;Kang, Eun Sil;Seo, Han Geuk
英文名：Alisma orientale（Sam.）泽泻（Alismataceae）是一种原产于北方和东亚的中草药，具有利尿、降血脂、抗炎、抗糖尿病等作用。材料和方法：用0.5mM棕榈酸酯处理HepG 2细胞以产生非酒精性脂肪性肝病（NAFLD）的细胞模型。使用这种细胞模型，AEAO（100 μ g/mL）对长链饱和脂肪酸诱导的细胞损伤的细胞保护作用进行了评估，通过测量脂肪变性，ROS积累，和apoptosis.Results：AEAO显着衰减棕榈酸诱导的细胞内脂肪变性和细胞损伤分别高达54和33%。棕榈酸诱导的细胞内活性氧（ROS）和活性醛的水平显着降低AEAO的存在下，分别为40和75%，这表明氧化应激在棕榈酸诱导的损伤中起作用。AEAO抑制棕榈酸介导的c-Jun NH 2-末端激酶（JNK）的活化，JNK是一种与NAFLD相关的激酶。通过SP 600125抑制JNK或加入AEAO显著减少棕榈酸诱导的脂肪变性、ROS积累和凋亡，表明AEAO对棕榈酸诱导的细胞损伤的保护作用是由于阻断ROS激活的JNK信号传导。AEAO在细胞脂肪变性和ROS产生中的组合特性有利于治疗NAFLD，其包括复杂的代谢变化，使得单一靶点的调节通常不足以实现所需的治疗效果。
Context: Alisma orientale (Sam.) Juzepczuk (Alismataceae) is an indigenous medicinal herb that has been traditionally used for diuretic, hypolipidemic, anti-inflammatory, and antidiabetic proposes in northern and eastern Asia.Objective: This study examined the mechanisms underlying the cytoprotective effect of an aqueous extract of A. orientale (AEAO) against long-chain saturated fatty acid-induced cellular injury.Materials and methods: HepG2 cells were treated with 0.5 mM palmitate to generate a cellular model of nonalcoholic fatty liver disease (NAFLD). Using this cellular model, the cytoprotective effect of AEAO (100 mu g/mL) against long-chain saturated fatty acid-induced cellular injury was evaluated by measuring the steatosis, ROS accumulation, and apoptosis.Results: AEAO significantly attenuated palmitate-induced intracellular steatosis and cellular damage up to 54 and 33%, respectively. Palmitate-induced intracellular levels of reactive oxygen species (ROS) and reactive aldehydes were significantly reduced in the presence of AEAO to 40 and 75%, respectively, suggesting that oxidative stress plays a role in the palmitate-induced damage. AEAO inhibited the palmitate-mediated activation of c-Jun NH2-terminal kinase (JNK), a kinase that is correlated with NAFLD. Inhibition of JNK by SP600125 or addition of AEAO significantly reduced palmitate-induced steatosis, ROS accumulation, and apoptosis, indicating that the protective effects of AEAO against palmitate-induced cellular damage result from blocking ROS-activated JNK signaling.Discussion and conclusion: The combined properties of AEAO in cellular steatosis and ROS production are beneficial for treating NAFLD, which includes complex metabolic changes, such that modulation of a single target is often not sufficient to achieve the desired therapeutic effect.