Asset Details
Do you wish to reserve the book?
硫氧还蛋白还原酶抑制剂乙烷硒啉逆转顺铂耐药及其机制研究
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
硫氧还蛋白还原酶抑制剂乙烷硒啉逆转顺铂耐药及其机制研究
Do you wish to request the book?
硫氧还蛋白还原酶抑制剂乙烷硒啉逆转顺铂耐药及其机制研究
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
硫氧还蛋白还原酶抑制剂乙烷硒啉逆转顺铂耐药及其机制研究
2017
Overview
目的：研究凋亡调控相关蛋白来了解顺铂耐药成因,同时考察乙烷硒啉（Ethaselen）在K562耐药细胞中逆转顺铂耐药的作用,并初步探讨其作用机制。创新点：首次研究乙烷硒啉在逆转顺铂耐药中的作用,且此作用与乙烷硒啉诱导细胞凋亡相关。方法：通过长时间脉冲诱导得到顺铂耐药K562细胞,并观察耐药细胞形态及倍增时间。采用MTT法考察乙烷硒啉、顺铂及其联用组在不同细胞株间的生长抑制作用。流式细胞术分析细胞凋亡情况以及细胞内活性氧（ROS）水平。最后,通过蛋白质免疫印迹（Western blot）考察凋亡调控相关蛋白水平的变化。结论：脉冲诱导得到的K562耐药细胞对顺铂的耐受性是原K562细胞的5.34倍。形态学观察发现,耐药细胞体积增大,粘附性进一步降低。乙烷硒啉与顺铂联用表现出协同效应。当加入少量的乙烷硒啉（顺铂与乙烷硒啉的摩尔比率为10：1）,顺铂作用K562耐药细胞的半抑制浓度（IC50）值可以减少21倍。流式细胞术及Western blot表明,乙烷硒啉能够诱导耐药细胞凋亡。其逆转顺铂耐药主要是通过调控Bcl-2及Bax蛋白比例以及通过提高细胞内活性氧水平引起线粒体通透转运孔道（PTP）蛋白孔道的形成来促使释放细胞色素c,进而引起Caspase凋亡途径。
