Bussière F I, Tridon A, Zimowska W, Mazur A, Rayssiguier Y
Centre de Recherches en Nutrition Humaine d'Auvergne, Unité Maladies Métaboliques et Micronutriments, INRA, Theix, 63122 St-Genès-Champanelle, France.
Life Sci. 2003 Jun 13;73(4):499-507. doi: 10.1016/s0024-3205(03)00291-1.
The importance of the inflammatory process in the pathology of experimental Mg-deficiency has been reconsidered but the sequence of events leading to inflammatory response remains unclear. In this study, the effect of Mg-deficiency on complement system by measuring total C3 concentration, mRNA abundance for rat pre-pro complement C3 in liver by RT-PCR, complement haemolytic activity and C3 activation by Western Blot was studied. Weaning male Wistar rats were fed either Mg-deficient or control experimental diets for 2 or 8 days. At 8 days, a characteristic inflammatory response of Mg-deficiency including hyperaemia, leukocytosis and enlarged spleen was accompanied by an increase in the total C3 quantity in plasma. Moreover, at 8 days, RT-PCR analysis indicated higher level of mRNA rat pre-pro complement C3 in liver from Mg-deficient rats compared to control rats. Even if the inflammatory syndrome was not observed in rats after 2 days, total plasma C3 was shown to be significantly increased as compared to total plasma C3 level in control rats. Because of the high variability of complement haemolytic activity values in Wistar rats, weaning male Sprague-Dawley rats were used in a second experiment. At 8 days, the inflammatory response of Sprague-Dawley rats was accompanied by an increase in total C3 quantity and by a higher haemolytic activity. The Western Blot technique failed to display distinct bands resulting from C3 cleavage in plasma from Mg-deficient rats. Since, the complement C3 is a positive acute phase reactant, the elevation of C3 indicates that the modification of inflammatory response is an early event of Mg-deficiency. However, complement activation does not appear to be involved in the acute phase of the deficiency.
炎症过程在实验性镁缺乏病理学中的重要性已被重新审视,但导致炎症反应的一系列事件仍不清楚。在本研究中,通过测量总C3浓度、用逆转录聚合酶链反应(RT-PCR)检测大鼠肝脏中前体补体C3的mRNA丰度、补体溶血活性以及用蛋白质印迹法检测C3激活情况,研究了镁缺乏对补体系统的影响。将断乳雄性Wistar大鼠分别喂食缺镁或对照实验饮食2天或8天。在第8天,镁缺乏的典型炎症反应,包括充血、白细胞增多和脾脏肿大,伴随着血浆中总C3量的增加。此外,在第8天,RT-PCR分析表明,与对照大鼠相比,缺镁大鼠肝脏中大鼠前体补体C3的mRNA水平更高。即使在2天后大鼠未观察到炎症综合征,但与对照大鼠的血浆总C3水平相比,血浆总C3仍显著增加。由于Wistar大鼠补体溶血活性值的高度变异性,在第二个实验中使用了断乳雄性Sprague-Dawley大鼠。在第8天,Sprague-Dawley大鼠的炎症反应伴随着总C3量的增加和更高的溶血活性。蛋白质印迹技术未能显示缺镁大鼠血浆中C3裂解产生的明显条带。由于补体C3是一种阳性急性期反应物,C3的升高表明炎症反应的改变是镁缺乏的早期事件。然而,补体激活似乎不参与缺乏的急性期。