破骨细胞与奶牛产乳热  

Osteoclast and milk fever

作　　者：张闯 顾建红[1] 马天洪 卞建春 刘学忠[1] 袁燕[1] 刘宗平[1] 

机构地区：[1]扬州大学兽医学院/江苏省动物重要疫病与人兽共患病防控协同创新中心,江苏扬州225009

出　　处：《畜牧与兽医》2017年第11期133-136,共4页Animal Husbandry & Veterinary Medicine

基　　金：国家自然科学基金项目(31302154;31672620;31372495);江苏省高校自然科学研究项目(13KJB230002);高校博士点基金(新教师类)(2O13325O12O0O2);江苏高校优势学科建设工程资助项目

摘　　要：奶牛产乳热是奶牛围产期的多发病,在养殖生产中造成了重大危害。研究发现,产乳热的发生与分娩前后血钙浓度降低有关。甲状旁腺激素(PTH)、降钙素(CT)和1α,25-(OH)_2D_3可直接或间接地调控破骨细胞(OC)的形成、活化和骨吸收功能,从而调控骨钙动员和血钙浓度,很可能与产乳热的发生息息相关。本文就PTH、CT和1α,25-(OH)_2D_3在产乳热中调控OC的可能机制作一综述。Milk fever,a frequently occurring disease in periparturient dairy cows,can cause serious harm to cow industry.Many studies indicated that the milk fever is related to the decreasing of serum calcium in periparturient dairy cows.It is well known that parathyroid hormone（PTH）,calcitonin（CT） and 1α,25-（OH）2D3 can regulate the formation,activation and bone resorption of osteoclast（OC） directly or indirectly,and thus regulate bone calcium mobilization and serum calcium concentration.The factors are likely to be related to the development of milk fever.This article summarizes the possible mechanisms of OC in milk fever under PTH,CT and 1α,25-（OH）2D3.

关 键 词：产乳热 血钙 破骨细胞 甲状旁腺激素 1α 25-(OH)2D3 

分 类 号：S858.23[农业科学—临床兽医学]