全站搜索
点评详情
 
点评分类
 
 
商品搜索
 
 
当前位置
点评详情
发布于:2018-7-20 11:02:03  访问:7 次 回复:0 篇
版主管理 | 推荐 | 删除 | 删除并扣分
H of therapy with EPA. ** indicates a important difference (p < 0.01) compared
These eicosanoids inhibit the activity of Akt/pkB kinase expression that reduces the PGE2 level [5] and have contrasting properties to PGE2, such as anti-inflammatory, anti-proliferation and proapoptosis [19, 39]. In addition, EPA treatment has been found to induce cell apoptosis via arresting cell cycle in pancreatic cancer cells [40]. This reduced the level of anti-apoptotic bcl-2 protein expression in human leukaemia cells [41]. Chi et al. have shown that EPA induced cell apoptosis activation via p53 dependent Fas/FasL pathway in hepatoma cells [42]. The role of EPA in the modulation of gene expression and activation of caspases involved in cancer cell apoptosis has also been reported [43, 44]. Furthermore, Fukui et al. have shown both in vitro and in vivo that the anti-cancer effects of EPA is associated with the cell death resulted from the accumulation of ROS in the cancer cells [17]. Studies have also shown that EPA and DHA induced apoptosis of colon cancer cells through GDC-0941 biological activity mitochondrial pathway involving a change of mitochondrial membrane potential (MMP), and the release of cytochrome c and other pro-apoptotic factors leading to cell death. have shown both in vitro and in vivo that the anti-cancer effects of EPA is associated with the cell death resulted from the accumulation of ROS in the cancer cells [17]. Studies have also shown that EPA and DHA induced apoptosis of colon cancer cells through mitochondrial pathway involving a change of mitochondrial membrane potential (MMP), and the release of cytochrome c and other pro-apoptotic factors leading to cell death. In addition, it has been reported that EPA treatment in vitro [17, 45, 46] and FO supplementation in vivo [47, 48] could increase ROS and Ca2+ levels in mitochondria and disrupt mitochondrial membranepotential leading to cell apoptosis in various human and rat cancer cells. To investigate whether the proapoptotic effect of EPA and krill oil extract in the present study was through mitochondrial pathway, we evaluated the changes in MMP after 48 h of treatment. It was found that there was a significant increase in the depolarization of mitochondria membrane in the cells treated with krill oil extract, and this was correlated with the number of apoptotic cells in the three cell lines (Figs. 4 5). However treatment with EPA or DHA did not show significant effect on MMP as krill oil extract (Fig. 5, data on DHA not shown). The results from the current study on MMP suggest that other components of the krill oil extract may play a role in the alteration of MMP, and the EPA induced cell apoptosis was possibly through other mechanisms rather than mitochondrial pathway. Further studies are required to fully understand the mechanisms underlying the pro-apoptotic effects of krill oil extract and whether other mechanistic pathways such as changes in cell cycle, signalling receptors, intracellular Ca2+ balance, and induced stress PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/25420080 in endoplasmic reticulum etc. also play a part [49]. Studies have shown the anti-cancer effect of PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28346523 DHA on quite a few cancer cell kinds such as colorectal cells [13, 50, 51]. DHA was identified to cut down cell proliferation a lot more effectively than EPA by Schonberg et al.
共0篇回复 每页10篇 页次:1/1
共0篇回复 每页10篇 页次:1/1
我要回复
回复内容
验 证 码
看不清?更换一张
匿名发表 
脚注信息
版权所有 Copyright(C)2010-2017  河北臣远体育发展有限公司