An in vitro study of Endoplasmic Reticulum Stress and ATF4 apoptosis signal pathways induced by Palm.docVIP

下载本文档

4
0
约1.07万字
约 15页
2016-11-29 发布于河北
举报
版权申诉

An in vitro study of Endoplasmic Reticulum Stress and ATF4 apoptosis signal pathways induced by Palm.doc

1、本文档共15页，可阅读全部内容。
2、原创力文档（book118）网站文档一经付费（服务费），不意味着购买了该文档的版权，仅供个人/单位学习、研究之用，不得用于商业用途，未经授权，严禁复制、发行、汇编、翻译或者网络传播等，侵权必究。
3、本站所有内容均由合作方或网友上传，本站不对文档的完整性、权威性及其观点立场正确性做任何保证或承诺！文档内容仅供研究参考，付费前请自行鉴别。如您付费，意味着您自己接受本站规则且自行承担风险，本站不退款、不进行额外附加服务；查看《如何避免下载的几个坑》。如果您已付费下载过本站文档，您可以点击这里二次下载。
4、如文档侵犯商业秘密、侵犯著作权、侵犯人身权等，请点击“版权申诉”（推荐），也可以打举报电话：400-050-0827(电话支持时间：9:00-18:30)。
5、该文档为VIP文档，如果想要下载，成为VIP会员后，下载免费。
6、成为VIP后，下载本文档将扣除1次下载权益。下载后，不支持退款、换文档。如有疑问请联系我们。
7、成为VIP后，您将拥有八大权益，权益包括：VIP文档下载权益、阅读免打扰、文档格式转换、高级专利检索、专属身份标志、高级客服、多端互通、版权登记。
8、VIP文档为合作方或网友上传，每下载1次，网站将根据用户上传文档的质量评分、类型等，对文档贡献者给予高额补贴、流量扶持。如果你也想贡献VIP文档。上传文档

An in vitro study of Endoplasmic Reticulum Stress and ATF4 apoptosis signal pathways induced by Palm

软脂酸钠体外诱导肝细胞内质网应激及ATF4细胞凋亡信号通路初步探讨宁波沈薇（重庆医科大学附属第二医院，400010） An in vitro study of Endoplasmic Reticulum Stress and ATF4 apoptosis signal pathways induced by Palmitate sodium on Hepatocytes Bo Ning, Wei Shen (The second Affiliated Hospital of Chongqing Medical University, 400010) Abstract Backgroud Saturated fatty acid is a strong apoptosis inducer of hepatocytes. The mechanisms remain to be clarified. Our aims were to investigate the role of endoplasmic reticulum stress (ER Stress) in the saturated fatty acid induced hepatocytes apoptosis. Methods The hepatocytes steatosis was established by L02 hepatocytes and palmitate sodium co-culturing. Cell viability and apoptosis were tested by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay and Annexin V/PI flow cytometry. MDA (malonaldehyde) and GSSG measurement were used to analyze lipid peroxidation. ER stress and apoptosis signaling were estimate by ATF4 mRNA and protein level determination. Reduced glutathione was applied as antioxidants to explore the role of lipid peroxidation in palmitate sodium induced apoptosis. Results Cell viability and apoptosis assay revealed that palmitate sodium induce hepatocytes apoptosis in a concentration and time depending manner. IC50 of palmitate sodium is 59.85umol/L. A significant cell protective effect can be detected after reduced glutathione was applied (P0.05). MDA and GSSG measurement verified an increased lipid peroxidation and significant extenuation after reduced glutathione was applied. ATF4 mRNA began to increase after 2 hours co-culturing and reached its peak after 12 hours at a level of 2.7 folds more than baseline. When reduced glutathione was applied, a dramatic reduction of both ATF4 mRNA and protein can be noticed. Conclusions Excessive cytoplasm lipid accumulation and following ER stress are the key events which mediate the palmitate sodium induced hepatocytes apoptosis. Lipid peroxidation is the main factor which provokes the ER stress a