Nutritional regulation of immunosenescence for heart health.
Nutritional regulation of immunosenescence for heart health.
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DOI：
10.1016/j.jnutbio.2004.10.001
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发表时间：
2005-02
期刊：
影响因子：
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通讯作者：
R. Watson;S. Zibadi;R. Vazquez;D. Larson
中科院分区：
文献类型：
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作者：
R. Watson;S. Zibadi;R. Vazquez;D. Larson
通过增加炎性细胞因子的免疫衰老可能在促进心脏感染和心力衰竭中发挥关键的调节作用。基于最近的证据，我们假设细胞因子极化由于老化直接失调成纤维细胞，导致改变心脏结构和功能障碍。一些膳食脂肪酸应改善升高的炎性细胞因子，从而延缓心脏病理，结构胶原蛋白的损失和心力衰竭的过早死亡。例如，T辅助细胞（Th）2细胞的细胞因子水平在老年人中非常高，这些老年人由于对心肌营养病原体的抵抗力受到抑制而增加了心脏病。此外，这类炎性细胞因子使成纤维细胞失调，从而减少胶原蛋白合成，削弱肌肉结构和心脏泵功能，导致心力衰竭和高血压。因此，补充n-3多不饱和脂肪酸（PUFA）或共轭亚油酸，通过减少Th 2和增加Th 1细胞因子，可以提供一个明智的和广泛可用的手段来治疗，甚至预防过度的炎性细胞因子及其心脏毒性作用。另一方面，饮食中的n-6 PUFA可能会促进老年人的细胞因子极化，加剧与年龄相关的心脏功能障碍。
Immunosenescence via increased inflammatory cytokines may play key regulatory roles in facilitating cardiac infections and heart failure. Based upon recent evidence, we hypothesize that cytokine polarization due to aging directly dysregulates fibroblasts, leading to altered cardiac structure and dysfunction. Some dietary fatty acids should ameliorate heightened inflammatory cytokines thereby retarding cardiac pathology, loss of structural collagen and premature death from heart failure. For example, T-helper (Th) 2 cells' cytokine levels are very high in seniors who have increased heart disease due to suppressed resistance to cardiotrophic pathogens. In addition, such inflammatory cytokines deregulate fibroblasts, thus reducing collagen synthesis, weakening muscle structure and heart pump function for heart failure and hypertension. Therefore, supplementation with n-3 polyunsaturated fatty (PUFA) or conjugated linoleic acids, by reducing Th2 and increasing Th1 cytokines, may provide a sensible and widely available means to treat and even prevent excessive inflammatory cytokines and their cardiotoxic effects. On the other hand, dietary n-6 PUFA may promote cytokine polarization in seniors, exacerbating age-related heart dysfunction.