Weglicki W B, Stafford R E, Freedman A M, Cassidy M M, Phillips T M
Department of Medicine, George Washington University Medical Center, Washington, DC 20037.
Am J Physiol. 1993 Mar;264(3 Pt 1):C723-6. doi: 10.1152/ajpcell.1993.264.3.C723.
Antioxidant treatment with alpha-tocopherol did not affect the level of the "inflammatory cytokines" in Mg-deficient animals, although it diminished the extent of the myocardial lesions. In another group of Mg-deficient animals chloroquine treatment diminished significantly the levels of circulating cytokines (interleukin-1, interleukin-6, and tumor necrosis factor-alpha) and also resulted in a major decrease in myocardial lesions. These results raise the question of the role of these inflammatory cytokines in the formation of lesions in Mg-deficient myocardium. Because these cytokines are able to stimulate free radical production in various cell types, we postulate that Mg deficiency involves free radical mechanisms that can be amplified by inflammatory cytokines; whether these cytokines initiate lesion formation is unclear. Although our data do not confirm either possibility, we submit that these results implicate a role for the inflammatory cytokines in the cardiac pathology of Mg deficiency.
用α-生育酚进行抗氧化治疗对缺镁动物体内“炎性细胞因子”的水平没有影响，尽管它减轻了心肌损伤的程度。在另一组缺镁动物中，氯喹治疗显著降低了循环细胞因子（白细胞介素-1、白细胞介素-6和肿瘤坏死因子-α）的水平，并且还导致心肌损伤大幅减少。这些结果引发了关于这些炎性细胞因子在缺镁心肌损伤形成中所起作用的问题。由于这些细胞因子能够刺激多种细胞类型产生自由基，我们推测缺镁涉及自由基机制，而炎性细胞因子可以放大这种机制；目前尚不清楚这些细胞因子是否引发损伤形成。尽管我们的数据并未证实这两种可能性中的任何一种，但我们认为这些结果表明炎性细胞因子在缺镁的心脏病理学中发挥了作用。
