首页> 外文期刊>International immunopharmacology >Pharmacological and biochemical studies on the role of free radicals during stress-induced immunomodulation in rats.
【24h】

Pharmacological and biochemical studies on the role of free radicals during stress-induced immunomodulation in rats.

机译:自由基在大鼠应激诱导的免疫调节中的作用的药理和生化研究。

获取原文
获取原文并翻译 | 示例
获取外文期刊封面目录资料

摘要

The present study was designed to evaluate the role of free radicals in restraint stress (RS)-induced modulation of immune responses in rats. RS significantly suppressed both humoral and cell-mediated immune responses as evidenced by reduced (a) anti-SRBC antibody titre (b) splenic Plaque Forming Cell counts, (c) footpad thickness response, and (d) IFN-gamma and IL-4 levels. Assay for oxidative stress markers in blood showed that there was significant enhancement in plasma corticosterone and products of lipid peroxidation, viz. malondialdehyde and lowered reduced glutathione levels on exposure to RS. Further, this was associated with decreased antioxidant enzyme activity, viz. superoxide dismutase and catalase. These RS-induced changes in immunological and oxidative stress markers were markedly attenuated by pretreatment with the antioxidants, L-ascorbic acid (100 and 200 mg/kg) and alpha-tocopherol (30 and 60 mg/kg), by differential degrees. The combination of L-ascorbic acid and alpha-tocopherol was shown to have synergistic effects on reversal of these RS-induced effects. The results suggest that reactive oxygen species may be involved in stress-induced immunomodulation.
机译:本研究旨在评估自由基在约束应激(RS)诱导的大鼠免疫反应调节中的作用。 RS显着抑制了体液和细胞介导的免疫反应,如降低的(a)抗SRBC抗体滴度(b)脾脏斑块形成细胞计数,(c)足垫厚度反应以及(d)IFN-γ和IL-4所证明水平。血液中氧化应激标志物的测定表明,血浆皮质酮和脂质过氧化产物明显增强。丙二醛和降低降低的谷胱甘肽水平,暴露于RS。此外,这与抗氧化酶活性降低有关。超氧化物歧化酶和过氧化氢酶。这些RS诱导的免疫和氧化应激标志物的变化通过抗氧化剂,L-抗坏血酸(100和200 mg / kg)和α-生育酚(30和60 mg / kg)的预处理而被显着减弱。 L-抗坏血酸和α-生育酚的组合显示出对逆转这些RS诱导的作用具有协同作用。结果表明活性氧可能参与应激诱导的免疫调节。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号