It is well known that the dairy cow production is very sensitive to environmental factors, including high temperature, high humidity and radiant heat sources. High temperature-induced heat stress is the main environmental factor that causes oxidative stress and apoptosis, which affects the development of mammary glands in dairy cows. Dihydromyricetin (DMY) is a nature flavonoid compound extracted from Ampelopsis grossedentata; it has been shown to have various pharmacological functions, such as anti-inflammation, antitumor and liver protection. The present study aims to evaluate the protective effect of DMY on heat stress-induced dairy cow mammary epithelial cells (DCMECs) apoptosis and explore the potential mechanisms. The results show that heat stress triggers heat shock response and reduces cell viability in DCMECs; pretreatment of DCMECs with DMY (25 μM) for 12 h significantly alleviates the negative effects of heat stress on cells. DMY can provide cytoprotective effects by suppressing heat stress-caused mitochondrial membrane depolarization and mitochondrial dysfunction, Bax and Caspase 3 activity, and modulation of oxidative enzymes, thereby preventing ROS production and apoptosis in DCMECs. Importantly, DMY treatment could attenuate heat stress-induced mitochondrial fragmentation through mediating the expression of mitochondrial fission and fusion-related genes, including Dynamin related protein 1 (Drp1), Mitochondrial fission 1 protein (Fis1), and Mitofusin1, 2 (Mfn1, 2). Above all, our findings demonstrate that DMY could protect DCMECs against heat stress-induced injury through preventing oxidative stress, the imbalance of mitochondrial fission and fusion, which provides useful evidence that DMY can be a promising therapeutic drug for protecting heat stress-induced mammary glands injury and mastitis.

众所周知，奶牛的生产对环境因素非常敏感，包括高温，高湿和辐射热源。高温引起的热应激是引起氧化应激和细胞凋亡的主要环境因素，其影响奶牛的乳腺发育。二氢杨梅素（DMY）是从毛果安眠草中提取的天然类黄酮化合物。它已被证明具有多种药理功能，例如抗炎，抗肿瘤和保护肝脏。本研究旨在评估DMY对热应激诱导的奶牛乳腺上皮细胞（DCMEC）凋亡的保护作用，并探讨其潜在机制。结果表明，热应激会触发热激反应并降低DCMEC中的细胞活力。用DMY（25μM）对DCMEC预处理12 h可以显着减轻热应激对细胞的负面影响。DMY可以通过抑制热应激引起的线粒体膜去极化和线粒体功能障碍，Bax和Caspase 3活性以及氧化酶的调节来提供细胞保护作用，从而防止DCMEC中的ROS产生和细胞凋亡。重要的是，DMY处理可以通过介导线粒体裂变和融合相关基因的表达来减轻热应激诱导的线粒体片段化，包括动力蛋白相关蛋白1（Drp1），线粒体裂变1蛋白（Fis1）和线粒体1、2（Mfn1、2 ）。最重要的是，我们的发现表明DMY可以通过防止氧化应激来保护DCMEC免受热应激诱导的伤害，