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首页> 外文期刊>Archives of Toxicology >Lanthanum chloride reduces lactate production in primary culture rat cortical astrocytes and suppresses primary co-culture rat cortical astrocyte-neuron lactate transport
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Lanthanum chloride reduces lactate production in primary culture rat cortical astrocytes and suppresses primary co-culture rat cortical astrocyte-neuron lactate transport

机译:氯化镧在原发性培养大鼠皮质星形胶质细胞中减少乳酸乳酸盐,抑制初级共同培养大鼠皮质星形细胞 - 神经元乳酸转运

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摘要

Lanthanum (La) can impair learning memory and induce behavioral abnormalities in animals. However, the mechanism underlying these adverse effects of La is still elusive. It has been demonstrated that lactate derived from astrocytes is the major energy source for neurons during long-term memory (LTM) formation and the deficiency of lactate supply can result in LTM damage. However, little work has been done with respect to the impact of La on the lactate production in astrocytes and astrocyte-neuron lactate transport (ANLT). Herein, experiments were undertaken to explore if there was such an adverse effect of La. Primary culture rat cortical astrocytes and primary co-culture rat cortical astrocyte-neuron were treated with (0.125, 0.25 and 0.5 mM) lanthanum chloride (LaCl3) for 24 h. The results showed that LaCl3 treatment significantly downregulated the mRNA and protein expression of glucose transporter 1 (GLUT1), glycogen synthase (GS), glycogen phosphorylase (GP), lactate dehydrogenase A (LDHA), and monocarboxylate transporter 1, 2 and 4 (MCT 1 2 and 4); upregulated the mRNA and protein expression of lactate dehydrogenase B (LDHB); and decreased the glycogen level, total LDH and GP activity, GS/p-GS ratio and lactate contents. Moreover, rolipram (20, 40 mu M) or forskolin (20, 40 mu M) could increase the lactate content by upregulating GP expression and the GS/p-GS ratio, as well as antagonize the effects of La. These results suggested that La-induced learning-memory damage was probably related to its suppression of lactate production in astrocytes and ANLT. This study provides some novel clues for clarifying the mechanism underlying the neurotoxicity of La.
机译:镧(LA)可以损害学习记忆并诱导动物的行为异常。然而,洛杉矶这些不利影响的机制仍然难以捉摸。已经证明,来自星形胶质细胞的乳酸盐是长期记忆(LTM)形成期间神经元的主要能源,并且乳酸乳酸供应的缺乏可能导致LTM损伤。然而,对La对星形胶质细胞和星形胶质细胞 - 神经元乳酸转运(ANLT)的乳酸盐产生的影响,已经完成了一点的工作。本文中,进行实验以探索LA的不良反应。原发性培养大鼠皮质星形胶质细胞和初级共培养大鼠皮质星形细胞 - 神经元用(0.125,0.25和0.5mM)氯化镧(LACL3)进行24个H。结果表明,LacL3处理显着下调葡萄糖转运蛋白1(Glut1),糖原合酶(Gs),糖原磷酸化酶(GP),乳酸脱氢酶A(LDHA)和单羧酸盐转运蛋白1,2和4的mRNA和蛋白表达(MCT 1 2和4);上调乳酸脱氢酶B(LDHB)的mRNA和蛋白质表达;并降低糖原水平,总量LDH和GP活性,GS / P-GS比和乳酸含量。此外,Rolipram(20,40μm)或叉醇(20,40μm)可以通过上调GP表达和GS / P-GS比率来增加乳酸含量,以及拮抗La的效果。这些结果表明La诱导的学习记忆损坏可能与其抑制星形胶质细胞和ANLT中的乳酸生成有关。本研究提供了一些新的线索,用于澄清La神经毒性的机制。

著录项

  • 来源
    《Archives of Toxicology》 |2018年第4期|共13页
  • 作者单位

    China Med Univ Sch Publ Hlth Dept Toxicol 77Puhe Rd Shenyang North New Area Shenyang 110122;

    China Med Univ Sch Publ Hlth Dept Toxicol 77Puhe Rd Shenyang North New Area Shenyang 110122;

    China Med Univ Sch Publ Hlth Dept Toxicol 77Puhe Rd Shenyang North New Area Shenyang 110122;

    China Med Univ Sch Publ Hlth Dept Toxicol 77Puhe Rd Shenyang North New Area Shenyang 110122;

    China Med Univ Sch Publ Hlth Dept Toxicol 77Puhe Rd Shenyang North New Area Shenyang 110122;

    China Med Univ Sch Publ Hlth Dept Toxicol 77Puhe Rd Shenyang North New Area Shenyang 110122;

    China Med Univ Sch Publ Hlth Dept Toxicol 77Puhe Rd Shenyang North New Area Shenyang 110122;

    China Med Univ Sch Publ Hlth Dept Toxicol 77Puhe Rd Shenyang North New Area Shenyang 110122;

    China Med Univ Sch Publ Hlth Dept Toxicol 77Puhe Rd Shenyang North New Area Shenyang 110122;

    China Med Univ Sch Publ Hlth Dept Toxicol 77Puhe Rd Shenyang North New Area Shenyang 110122;

    China Med Univ Sch Publ Hlth Dept Toxicol 77Puhe Rd Shenyang North New Area Shenyang 110122;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 毒物学(毒理学);
  • 关键词

    Lanthanum; Lactate production; Astrocyte-neuron lactate transport; Long-term memory;

    机译:镧;乳酸生产;星形胶质细胞 - 神经元乳酸转运;长期记忆;

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