Boutros Cherif, Somasundar Ponnandai, Razzak Anthony, Helton Scott, Espat N Joseph
Department of Hepatobiliary and Surgical Oncology, Roger Williams Medical Center, 825 Chalkstone Ave, Prior 4, Providence, RI 02908, USA.
Arch Surg. 2010 Jun;145(6):515-20. doi: 10.1001/archsurg.2010.91.
Omega-3 (omega-3) fatty acids have been clinically and experimentally associated with the amelioration of chronic and acute inflammation; however, the mechanisms for these observations have not been well defined. During the past decade, laboratories of nutrition and inflammation have demonstrated that the anti-inflammatory activities of omega-3 fatty acids occur at least in part through the inhibition of macrophage-elaborated tumor necrosis factor production and through inactivation of the nuclear factor-kappaB signaling pathway subsequently altering proinflammatory cytokine transcription. These observations led to further experiments that support a role for omega-3 fatty acids in the restoration of apoptosis in various chemoresistant tumor models through a similar inactivation of the nuclear factor-kappaB signaling pathway. The potential for nutritional modulation of host inflammation has been an ongoing and expanding area of investigation. An increased emphasis has been placed on the potential for diet and dietary supplements to serve as modulators of host response to disease, injury, and infection.
ω-3脂肪酸在临床和实验上都与急慢性炎症的改善有关；然而，这些观察结果的机制尚未明确。在过去十年中，营养与炎症实验室表明，ω-3脂肪酸的抗炎活性至少部分是通过抑制巨噬细胞产生的肿瘤坏死因子以及使核因子-κB信号通路失活，进而改变促炎细胞因子转录来实现的。这些观察结果引发了进一步的实验，这些实验支持ω-3脂肪酸通过类似的核因子-κB信号通路失活，在各种化疗耐药肿瘤模型中恢复细胞凋亡方面发挥作用。宿主炎症的营养调节潜力一直是一个不断发展的研究领域。人们越来越重视饮食和膳食补充剂作为宿主对疾病、损伤和感染反应调节剂的潜力。
