Abstract：
During the periparturient period, lipolysis in adipose tissue (AT) mobilizes fatty acid reserves to meet high energy needs of dairy cows. This physiological response is accompanied by the synthesis and secretion of a plethora of proteins (adipokines) and lipid products that modulate metabolic functions. In the AT, lipolysis generates free radicals (FR), including reactive oxygen species, and leads to a remodeling process characterized by an inflammatory response. In the AT of healthy cows with adequate lipolytic responses, antioxidant defenses neutralize FR, and the inflammation associated with remodeling is rapidly resolved. The control of these processes is orchestrated by numerous inflammatory and oxidative stress (OS)-related pathways identified by recent transcriptomic and proteomic analyses. For example, parturition and the onset of lactation enhance the transcription and translation of complement and acute-phase proteins and, at the same time, enrich antioxidant defenses that neutralize FR, including Nrf2. However, in cows with exacerbated and protracted lipolysis, the production of FR rapidly depletes antioxidant systems, and OS develops. The harmful effects of OS in AT include activating inflammatory responses and inhibiting insulin signaling within AT. By intensifying AT inflammation, OS impairs adipocyte response to insulin. This leads to a vicious circle where OS exacerbates AT lipolysis and inflammation, which further promotes OS. This review summarizes current knowledge on the mechanisms that modulate AT inflammatory responses and OS during the periparturient period of dairy cows.
摘要：
在围产期,脂肪组织（AT）中的脂解动员脂肪酸储备以满足奶牛的高能量需求。这种生理反应伴随着调节代谢功能的过多蛋白质(脂肪因子)和脂质产物的合成和分泌。在AT,脂肪分解产生自由基（FR），包括活性氧，并导致以炎症反应为特征的重塑过程。在具有足够脂肪分解反应的健康奶牛的AT中，抗氧化剂防御中和FR，与重塑相关的炎症迅速解决。这些过程的控制是通过最近的转录组和蛋白质组分析鉴定的许多炎症和氧化应激（OS）相关途径协调的。例如,分娩和泌乳开始增强补体和急性期蛋白的转录和翻译，同时,丰富的抗氧化剂防御，中和FR，包括Nrf2。然而,在脂肪分解加剧和延长的奶牛中，FR的生产迅速耗尽抗氧化系统，和操作系统的发展。OS在AT中的有害作用包括激活炎症反应和抑制AT内的胰岛素信号传导。通过加强AT炎症，OS损害脂肪细胞对胰岛素的反应。这导致了一个恶性循环，OS加剧了AT脂解和炎症，这进一步促进了OS。这篇综述总结了当前有关奶牛围产期AT炎症反应和OS调节机制的知识。
