Tumor necrosis factor alpha inhibits in vitro bovine embryo development through a prostaglandin mediated mechanism

作     者：Lauren R Jackson Char E Farin Scott Whisnant 

作者机构：Department of Animal Science North Carolina State University PO Box 7621 Raleigh NC 27695-7621 USA 

出 版 物：《Journal of Animal Science and Biotechnology》 (畜牧与生物技术杂志（英文版）)

年 卷 期：2012年第3卷第1期

页      面：21-24页

核心收录：

学科分类：0710[理学-生物学] 0831[工学-生物医学工程（可授工学、理学、医学学位）] 090603[农学-临床兽医学] 0832[工学-食品科学与工程（可授工学、农学学位）] 1004[医学-公共卫生与预防医学(可授医学、理学学位)] 0905[农学-畜牧学] 0906[农学-兽医学] 09[农学] 0703[理学-化学] 0836[工学-生物工程] 

基　　金：supported by an assistantship from the Department of Animal Science North Carolina State University 

主　　题：tumor necrosis factor o bovine embryo indomethacin 

摘      要：Mastitis or other infectious diseases have been related to reduced fertility in cattle. Inflammatory cytokines such as tumor necrosis factor α （TNFα are released in response to infection and may have negative effects on embryo development, in the current study the effect of exposure to TNFα on the development of in vitro fertilized bovine embryos was examined. Indomethacin, a prostaglandin synthesis inhibitor, was used to determine if blockade of prostaglandin synthesis would alter the effects of TNFα Ovaries were obtained from a local abattoir and immature COC were isolated from 2-10 mm follicles, in vitro matured and fertilized. After fertilization, groups of presumptive zygotes were randomly placed into either control development medium, medium containing 25 ng/mL TNFα or medium containing 25 ng/mL TNFα plus 1 μg/mL indomethacin. The proportion of blastocysts formed was assessed at day 7 of culture. Fewer embryos exposed to TNFα alone reached the blastocyst stage （17.5 ± 2.4%, P 〈 0.01） compared with controls （30.5 ± 2.4%） or embryos developed in TNFα plus indomethacin （25.8 ± 2.8%）. There was no difference between control embryos and embryos developed in TNFα plus indomethacin. These results indicate that TNFα is inhibitory to the in vitro development of bovine embryos and that this inhibition may be mediated by prostaglandins because it can be blocked by indomethacin.