Dietary glutamine supplementation partly reverses impaired macrophage function resulting from overload training in rats.

Dietary glutamine supplementation partly reverses impaired macrophage function resulting from overload training in rats.
复制标题

DOI:
10.1123/ijsnem.2014-0118
复制
发表时间:
2015-04
影响因子:
2.5
通讯作者:
W. Xiao;Peijie Chen;Jingmei Dong;Ru Wang;Beibei Luo
W. Xiao;Peijie Chen;Jingmei Dong;Ru Wang;Beibei Luo
中科院分区:
医学2区
文献类型:
--
作者:
W. Xiao;Peijie Chen;Jingmei Dong;Ru Wang;Beibei Luo

文献摘要

被引文献

相似文献

本研究的目的是评估超负荷训练对大鼠腹腔巨噬细胞功能的影响,并验证体内补充谷氨酰胺将部分逆转超负荷训练诱导的这些细胞最终功能改变的假设。将40只雄性Wistar大鼠随机分为5组:对照组(C)、超负荷训练组(E1)、超负荷训练恢复1周组(E2)、补充谷氨酰胺组(EG1)、补充谷氨酰胺恢复1周组(EG2)。所有大鼠,除了那些放置在久坐不动的控制进行了11周的超负荷训练协议。测定大鼠血红蛋白、血清睾酮和皮质酮。测定腹腔巨噬细胞的趋化性、吞噬功能、细胞因子合成、活性氧产生等功能。结果表明,超负荷训练组血红蛋白、血清睾酮、皮质酮及体重均较对照组显著降低。同时,超负荷训练抑制了巨噬细胞的趋化能力(降低了31%,p = 0.003)、吞噬能力(降低了27%,p = 0.005)、活性氧(ROS)产生(降低了35%,p = 0.003)和细胞因子反应能力。补充谷氨酰胺可改善和逆转超负荷训练对巨噬细胞吞噬功能和细胞因子反应能力的影响。这些结果表明,超负荷训练损害了腹腔巨噬细胞的功能,这是必不可少的杀菌作用的巨噬细胞。这可能是超负荷训练导致免疫抑制的一种新机制。然而,补充谷氨酰胺可以部分逆转超负荷训练导致的巨噬细胞功能受损。
The aim of this study was to evaluate the effect of overload training on the function of peritoneal macrophages in rats, and to test the hypothesis that glutamine in vivo supplementation would partly reverse the eventual functional alterations induced by overload training in these cells. Forty male Wistar rats were randomly divided into 5 groups: control group (C), overload training group (E1), overload training and restore one week group (E2), glutamine-supplementation group (EG1), and glutamine-supplementation and restore 1-week group (EG2). All rats, except those placed on sedentary control were subjected to 11 weeks of overload training protocol. Blood hemoglobin, serum testosterone, and corticosterone of rats were measured. Moreover, the functions (chemotaxis, phagocytosis, cytokines synthesis, reactive oxygen species generation) of peritoneal macrophages were determined. Data showed that blood hemoglobin, serum testosterone, corticosterone and body weight in the overload training group decreased significantly as compared with the control group. Meanwhile, the chemotaxis capacity (decreased by 31%, p = .003), the phagocytosis capacity (decreased by 27%, p = .005), the reactive oxygen species (ROS) generation (decreased by 35%, p = .003) and the cytokines response capability of macrophages were inhibited by overload training. However, the hindering of phagocytosis and the cytokines response capability of macrophages induced by overload training could be ameliorated and reversed respectively, by dietary glutamine supplementation. These results suggest that overload training impairs the function of peritoneal macrophages, which is essential for the microbicidal actions of macrophages. This may represent a novel mechanism of immunodepression induced by overload training. Nonetheless, dietary glutamine supplementation could partly reverse the impaired macrophage function resulting from overload training.