绿茶多酚缓解氧化损伤奶牛乳腺上皮细胞炎症和凋亡的分子机制研究

氧化应激产生的大量活性氧（ROS）可诱导奶牛乳腺上皮细胞（BMECs）产生氧化损伤，降低机体免疫功能和炎症应答能力，导致细胞凋亡，降低奶牛生产性能。绿茶多酚（GTP）作为抗氧化剂可缓解奶牛围产期间产生的氧化应激。本研究选取健康BMECs，采用H2O2处理诱导BMECs产生氧化损伤，对比分析健康和氧化损伤BMECs中p38MAPK/NF-κB和p38MAPK/Cyt-c/AIF/caspase-3/p53通路中基因表达情况，确定其在氧化损伤BMECs炎症和凋亡中的作用；采用抑制p38MAPK，或敲除NFE2L2，添加GTP后，检测健康和氧化损伤BMECs中p38MAPK/NF-κB和p38MAPK/Cyt-c/AIF/caspase-3/ p53通路的表达情况，揭示出GTP缓解氧化损伤BMECs炎症和凋亡的分子机制。该研究可为绿茶多酚有效缓解因氧化应激诱导的炎性疾病提供理论基础和技术支撑。

Oxidative stress (OS) can induce oxidative damage in bovine mammary epithelial cells (BMECs) by generating a large number of reactive oxygen species (ROS), which reduce the immune function and inflammatory response, result in apoptosis of BMECs, and finally decrease the performance of dairy cows. Green tea polyphenols (GTP), as an antioxidants, can alleviate the oxidative stress during the perinatal period in dairy cows. The healthy BMECs are used and treated by H2O2 in this study. The role of p38MAPK/NF-κB and p38MAPK/Cyt-c/AIF/caspase-3/p53 pathways in inflammation and apoptosis of BMECs is determined by analyzing the expression of p38MAPK/NF-κB and p38MAPK/Cyt-c/ AIF/caspase-3/p53 pathways in healthy and oxidative damage cells. The mechanisms of GTP attenuate inflammation and apoptosis of oxidative stress-induced BMECs by regulating p38MAPK/NF-κB and p38MAPK/Cyt-c/AIF/caspase-3/p53 pathways is clarified by detecting the expression of p38MAPK/NF-κB and p38MAPK/Cyt-c/AIF/caspase-3/p53 pathways in both healthy and oxidative damage cells after GTP is added via inhibiting p38MAPK or knocking out NFE2L2. This study can provide theoretical and technical basis for effectively reducing the inflammatory diseases induced by oxidative stress.