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基于TGF-β1/p38MAPK/FN信号通路的放射性食管炎发病机制的研究

Pathogenesis of Radioactive Esophagitis Based on TGF-β1/p38MAPK/FN Signaling Pathway

  • 摘要:
    目的 从黏膜修复角度探讨放射性食管炎的发病机制,并明确是否与TGF-β1/p38MAPKs/FN信号通路相关。
    方法 HE染色法对放射性食管炎标本进行病理分析,Real-time PCR法检测标本FN、TGF-β1基因表达水平,Western blot法检测组织蛋白TGF-β1、p38、FN的表达。
    结果 SD大鼠发生放射性食管炎后第一周体质量、进食量、进水量明显下降(P < 0.05),第四周恢复;病理方面,第一、二周食管黏膜层破坏,第四周出现再生;黏膜相关细胞因子TGF-β1、FN与病理变化一致,TGF-β1、p38MAPK蛋白表达先上升后下降,而FN蛋白表达先下降后上升。
    结论 TGF-β1/p38MAPK/FN信号通路可能参与了其黏膜修复过程。

     

    Abstract:
    Objective To investigate the pathogenesis mechanism of radiation esophagitis from the perspective of mucosal regeneration and to determine whether it is associated with TGF-β1/p38MAPKs/FN signaling pathway.
    Methods The pathological analysis of esophageal specimens was performed by HE staining method. The expression of FN and TGF-β1 genes were observed by real time-PCR method, and the expression of tissue proteins TGF-β1, p38 and FN were detected by Western blot.
    Results The weights, food intakes and water intakes at the first week after the occurrence of radiation esophagitis were significantly decreased (P < 0.05) and recovered at the fourth week. The esophageal mucosa was destructed at the first and second weeks, and the regeneration occurred in the fourth weeks; TGF-β1 and p38MAPK protein expression increased first and then decreased, while FN protein expression decreased first and then increased.
    Conclusion The TGF-β1/p38MAPK/FN signaling pathway may be involved in the process of mucosal repair.

     

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