Protective effect of calcium deficiency on the inflammatory response in magnesium-deficient rats

Protective effect of calcium deficiency on the inflammatory response in magnesium-deficient rats
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DOI:
10.1007/s00394-002-0376-0
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发表时间:
2002-10-01
影响因子:
5
通讯作者:
Rayssiguier, Y
Rayssiguier, Y
中科院分区:
医学2区
文献类型:
--
作者:
Bussière, FI;Gueux, E;Rayssiguier, Y

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先前的研究表明,大鼠饮食中缺镁会导致明显的促炎作用。由于镁(Mg)经常作为天然钙(Ca)拮抗剂,因此可能存在镁缺乏的促炎作用可能是细胞外Mg2+/Ca2+拮抗作用减少的结果。因此,本研究的目的是评估膳食钙缺乏是否能改善镁缺乏大鼠的异常炎症反应。材料与方法将断奶雄性Wistar大鼠按饲粮镁、钙水平随机分为4组:缺钙组(对照组)、缺钙组(对照组)、缺钙组(缺钙组)、缺钙组(缺钙组)。分别饲喂8 d。结果与对照组相比,缺镁足钙大鼠血浆Mg浓度正常下降,而血浆Ca浓度未受影响。典型的炎症症状包括充血、白细胞增多和脾脏重量增加。此外,这些动物还表现出心脏脂质过氧化和血浆甘油三酯浓度的增加。在缺镁大鼠中,缺钙引起低钙血症,并对缺镁的促炎作用提供了显著的保护。这可以通过较低的炎症评分、预防白细胞增多和脾脏肿大来证明。钙缺乏对镁缺乏的炎症反应的保护作用伴随着脂质过氧化的显著减少和血浆甘油三酯浓度的正常化。综上所述,Ca参与了实验性缺镁的炎症反应,氧化应激和高甘油三酯血症是缺镁后大鼠急性期反应的结果。
Background Previous studies indicated that dietary Mg-deficiency in rats results in a marked pro-inflammatory effect. Since magnesium (Mg) frequently acts as a natural calcium (Ca) antagonist, the possibility exists that the pro-inflammatory effect of Mg-deficiency may be a consequence of a reduced extracellular Mg2+/Ca2+ antagonism. Aim of the study Thus, the aim of the study was to assess whether dietary Ca-deficiency improves the abnormal inflammatory response of Mg-deficient rats. Materials and methods Weaning male Wistar rats were randomly divided into 4 groups according to the dietary Mg and Ca as follows: Mg-adequate Ca-adequate (control), Mg-adequate Ca-deficient, Mg-deficient Ca-adequate, Mg-deficient Ca-deficient. Animals were fed the appropriate diets for 8 days. Results Mg-deficient Ca-adequate rats as compared to controls displayed the usual decrease in plasma Mg, whereas the plasma Ca concentration was unaffected. The classical symptoms of inflammation including hyperemia, increased number of blood leukocytes and increased spleen weight were observed. In addition, these animals also showed an increase in heart lipid peroxidation and in plasma triglyceride concentration. In Mg-deficient rats, Ca-deficiency induced hypocalcemia and offered a significant protection against the pro-inflammatory effect of Mg-deficiency. This was evidenced by lower inflammation scores, prevention of leukocytosis and of spleen enlargement. The protective effects of Ca-deficiency on the inflammatory response in Mg-deficiency was accompanied by significant reduction in lipid peroxidation and by a normalization of plasma triglyceride concentration. Conclusion All together, the results suggest that Ca is implicated in the inflammatory response of experimental Mg-deficiency and that oxidative stress and hypertriglyceridemia are the results of the acute phase response following Mg-deficiency in rats.