Ligustilide inhibits tumour necrosis factor-alpha-induced autophagy during C2C12 cells differentiation
Ligustilide inhibits tumour necrosis factor-alpha-induced autophagy during C2C12 cells differentiation
复制标题
藁本内酯抑制 C2C12 细胞分化过程中肿瘤坏死因子-α 诱导的自噬
DOI：
10.1016/j.biopha.2014.11.002
复制
发表时间：
2015-02-01
影响因子：
7.5
通讯作者：
Wei, Lianbo
中科院分区：
文献类型：
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作者：
Shi, Ying;Xiao, Liming;Wei, Lianbo
阿替利特被广泛认为是当归中最有效的生物活性成分。我们以前曾报道过藁本内酯在预防TNF-α诱导的细胞凋亡中的作用，并鉴定了自噬体簇的存在。然后，我们假设自噬可能导致肌肉损失，并且藁本内酯可以通过调节自噬过程来保护细胞纤维。本研究的目的是确定在TNF-α存在的情况下，藁本内酯对细胞分化过程中自噬调节的影响。然后，我们观察细胞内的形态学变化和自噬体的形成，用透射电子显微镜。通过免疫荧光法评估LC 3B表达，并通过western blot检测Atg-7、Atg-5、Atg-12和LC 3B表达水平。结果显示，在藁本内酯处理后，TNF-α诱导的自噬体的数量减少，伴随着Atg-7、Atg-5、Atg-12和LC 3B表达的减少，以及LC 3BII/I比率以浓度依赖性方式降低。我们的研究结果提供了证据支持藁本内酯对TNF-α诱导的自噬在肌管形成的保护作用。(C)2014年Elsevier Masson SAS。All rights reserved.
Ligustilide is widely thought to be the most potent bioactive constituent of Angelica sinensis. We have previously reported the role of ligustilide in preventing TNF-alpha-induced apoptosis and identified the presence of autophagosome clusters. Then, we hypothesised that autophagy may contribute to muscle loss and that ligustilide could protect cell fibres by regulating the autophagic process. The aim of this study was to identify the effects of ligustilide on autophagy regulation during cell differentiation in the presence of TNF-alpha. We then observed intracellular morphologic changes and autophagosome formation using transmission electron microscopy. LC3B expression was assessed by immunofluorescence and Atg-7, Atg-5, Atg-12 and LC3B expression levels were detected by western blot. The results revealed a reduction in the number of TNF-a-induced autophagosomes after ligustilide treatment accompanied by a decrease in Atg-7, Atg-5, Atg-12 and LC3B expression, as well as a reduction of the LC3BII/I ratio in a concentration-dependent manner. Our findings provide evidence supporting a protective effect of ligustilide against TNF-alpha-induced autophagy during myotubes formation. (C) 2014 Elsevier Masson SAS. All rights reserved.