中文摘要：

乳腺炎，感染由克积极的细菌引起了，在生产牛奶的哺乳动物生产乳房发炎和氧化损害。像使用费的受体(TLR2 ) 2 为入侵克积极的微生物的主人识别是重要的。在转基因的奶店山羊的 TLR2 的在表示上是为与克积极的细菌学习感染的各种各样的方面的一个有用模型，在 vivo.MethodsWe 在转基因的奶店山羊的过去表示的 TLR2。 Pam3CSK4 ，克积极的细菌的一个部件，由从使活跃之物 protein-1 ( AP-1 )的TLR2积极的转基因的山羊，和导致的在表示上刺激单核白血球巨噬细胞触发了 TLR2 信号小径， phosphatidylinositol 3-kinase ( PI3K )和抄写因素原子因素 kappa B ( NF-B )和有野类型的控制的信号 pathway.ResultsCompared 下游的发炎因素，各种各样的氧化压力相关的分子的大小显示出那 TLR2 ，什么时候 over-expresse 当 Pam3CSK4 被用来在 vivo 刺激耳朵织物时，转基因的山羊的 HO-1 蛋白质有结果显示的相对高的表示 level.ConclusionsThe 在山羊的氧化损害过去表示的 TLR2 被减少跟随 Pam3CSK4 刺激。为这减小的内在的机制是由 Nrf2 信号小径的激活的反氧化基因 HO-1 的增加的表示。

英文摘要：

Background： Mastitis, an infection caused by Gram-positive bacteria, produces udder inflammation and oxidative injury in milk-producing mammals. Toll-like receptor 2（TLR2） is important for host recognition of invading Grampositive microbes. Over-expression of TLR2 in transgenic dairy goats is a useful model for studying various aspects of infection with Gram-positive bacteria, in vivo.Methods： We over-expressed TLR2 in transgenic dairy goats. Pam3CSK4, a component of Gram-positive bacteria,triggered the TLR2 signal pathway by stimulating the monocytes-macrophages from the TLR2-positive transgenic goats, and induced over-expression of activator protein-1（AP-1）, phosphatidylinositol 3-kinase（PI3K） and transcription factor nuclear factor kappa B（NF-κB） and inflammation factors downstream of the signal pathway.Results： Compared with wild-type controls, measurements of various oxidative stress-related molecules showed that TLR2, when over-expressed in transgenic goat monocytes-macrophages, resulted in weak lipid damage, high level expression of anti-oxidative stress proteins, and significantly increased m RNA levels of transcription factor NF-E2-related factor-2（Nrf2） and the downstream gene, heme oxygenase-1（HO-1）. When Pam3CSK4 was used to stimulate ear tissue in vivo the HO-1 protein of the transgenic goats had a relatively high expression level.Conclusions： The results indicate that the oxidative injury in goats over-expressing TLR2 was reduced following Pam3CSK4 stimulation. The underlying mechanism for this reduction was increased expression of the anti-oxidation gene HO-1 by activation of the Nrf2 signal pathway.