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首页> 外文期刊>The Journal of toxicological sciences >Dexmedetomidine premedication attenuates concanavalin a-induced hepatitis in mice
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Dexmedetomidine premedication attenuates concanavalin a-induced hepatitis in mice

机译：右美托咪定的用药能减轻伴刀豆球蛋白A诱导的小鼠肝炎

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摘要

Activated T cells selectively induced by concanavalin A (Con A) in liver are subsequent efficient resolution of inflammation. Activated T cells infiltrating in liver combined with pro-inflammatory cytokines are the major causes in Con A-induced liver injury. In our study, C57/BL mice were injected with Con A combined with dexmedetomidine or not. ALT and AST in blood and histopathology of liver were measured. T cell infiltration in liver was examined by flow cytometry and pro-inflammatory cytokines including IL-6, IL-10, TNF-a, and IFN-y in blood were measured by ELISA. The mRNA level of CXCL10 was detected by RT-PCR and the protein level of NF-kB was measured by Western-blot. We found that dexmedetomidine alleviated Con A-induced liver injury by down-regulating levels of ALT and AST in blood and the severity of histopathology, which reflect the severity of hepatitis induced by Con A. In addition, pro-inflammatory cytokines in blood were attenuated by dexmedetomidine. Dexmedetomidine restrained the phosphorylation of NF-kB IicBa and P-65 dramatically which may participate in the regulation of cytokines secretion. Moreover, CXCL10 mRNA attenuated by dexmedetomidine in liver may result in the lower level of CD4+ T cells infiltration in liver. These results suggested that dexmedetomidine might be a potential compound in treating T cell-mediated liver injury.
机译：伴刀豆球蛋白A（Con A）在肝脏中选择性诱导的活化T细胞是炎症的后续有效解决方法。激活的T细胞在肝脏中浸润并结合促炎细胞因子是Con A诱导的肝损伤的主要原因。在我们的研究中，是否给C57 / BL小鼠注射Con A和右美托咪定联用。测量血液中的ALT和AST以及肝的组织病理学。通过流式细胞术检查肝脏中的T细胞浸润，并通过ELISA测量血液中的促炎细胞因子包括IL-6，IL-10，TNF-α和IFN-γ。 RT-PCR检测CXCL10的mRNA水平，Western-blot检测NF-kB的蛋白水平。我们发现右美托咪定通过下调血液中ALT和AST的水平以及组织病理学的严重程度减轻了Con A诱发的肝损伤，这反映了Con A诱发的肝炎的严重程度。此外，血液中的促炎细胞因子被减弱由右美托咪定。右美托咪定显着抑制了NF-kB IicBa和P-65的磷酸化，这可能参与细胞因子分泌的调节。此外，右美托咪定在肝脏中减弱的CXCL10 mRNA可能导致肝脏中CD4 + T细胞浸润的水平降低。这些结果表明右美托咪定可能是治疗T细胞介导的肝损伤的潜在化合物。

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