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首页> 外文期刊>Journal of chemical neuroanatomy >Human placental extract ameliorates cytokine and cytokine receptor signaling in the rat hippocampus upon Benzo[a]Pyrene exposure
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Human placental extract ameliorates cytokine and cytokine receptor signaling in the rat hippocampus upon Benzo[a]Pyrene exposure

机译：人的胎盘提取物在苯并[a]芘暴露时在大鼠海马中改善细胞因子和细胞因子受体信号传导

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Benzo[alpha]Pyrene (B[a]P) causes toxicity via Cytochrome P450 1A1 (CYP1A1) metabolic activity in the brain. Studies have shown that neuronal IL-2 and TNF-alpha are associated with the hippocampus development and regulation, but their association with the CYP1A1 activity remains unidentified. Limited action of human placental extract (HPE) in the activation of tissue repair and wound healing is known, but their role in B[a]P clearance in the hippocampus is not known so far. Our study has focused on two novel concepts: (1) association of CYP1A1 activity with the inflammatory response in the brain hippocampus and (2) role of HPE in the immunomodulatory mechanisms in the hippocampus upon B[a]P exposure at cytokine receptor and nuclear level. Intrathecal administration of different concentrations of B[a]P and HPE into male wistar rat pups has been conducted. An increased CYP1A1 activity was observed in the presence of 0.25 mu M B[a]P alone but in case of HPE followed by 0.25 mu M B[a]P, it was equal to control. Herein we report that 5 mu l of 0.1 gm HPE followed by 0.25 M B[a]P administration enabled down-regulation of IL-2 and TNF-alpha levels in the hippocampus thereby modulating TNFR2 and IL2R gamma(c) signals via NF-kappa B activation. Besides, localization of IL-2, TNF-alpha, IL2R gamma(c), TNFR1 and TNFR2 in the CA1, CA3 and DG regions of the hippocampus are also depicted. Altogether, these findings will project the clinical importance of HPE in the neuroinflammation suppression in the hippocampus developed due to B[a]P toxicity.
机译：苯并α-芘（B [A] P）通过细胞色素P450 1A1（CYP1A1）在脑中代谢活性引起毒性。研究表明，神经元IL-2和TNF-α与海马发育和调节有关，但它们与CYP1A1活性的关联仍未认定。人胎盘提取物（HPE）在组织修复和伤口愈合激活中的有限作用是已知的，但到目前为止，它们在海马中的B [A] P清除中的作用是未知的。我们的研究专注于两种新颖的概念：（1）CYP1A1活性与脑海马的炎症反应协会和（2）HPE在细胞因子受体和核对海马的免疫调节机制中的作用等级。已经进行了鞘内施用不同浓度的B [A] P和HPE进入雄性Wistar大鼠幼崽。在单独存在0.25μm[a] p的情况下，观察到增加的CYP1A1活性，但是在HPE之后，在0.25μmb[a] p的情况下，它等于对照。在此，我们报告的是，5μl0.1GMHPE，然后在海马中的下调IL-2和TNF-α水平的下调，从而通过NF-Kappa调节TNFr2和IL2Rγ（C）信号，从而调节0.25Mb的0.21Mb HPE。 B激活。此外，还描绘了IL-2，TNF-α，IL2Rγ（C），TNFR1和TNFR2的局部化，也描绘了海马的CA1，CA3和DG区域中的局部化。总的来说，这些发现将在由于B [A] P毒性引起的海马中发育的神经引征抑制中的HPE临床重要性。

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