Pathogenesis of Radioactive Esophagitis Based on TGF-β1/p38MAPK/FN Signaling Pathway
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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。
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关键词:
- TGF-β1/p38MAPK/FN信号通路 /
- 放射性食管炎 /
- 黏膜修复 /
- 细胞因子
Abstract:ObjectiveTo 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.
MethodsThe 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.
ResultsThe 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.
ConclusionThe TGF-β1/p38MAPK/FN signaling pathway may be involved in the process of mucosal repair.
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Competing interests: The authors declare that they have no competing interests.作者贡献张福鹏:课题设计及文章撰写赵晓燕、郝淑兰、樊桂玲、王爱荣:实验设计与操作李晓丽:统计分析刘丽坤:文章指导
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表 1 目的基因引物及探针
Table 1 Target gene primers and probes
表 2 放射性食管炎SD大鼠模型食管组织FN、TGF-β1 mRNA的表达
Table 2 Expression of FN and TGF-β1 mRNA in esophagus tissue of SD rat model of radiation esophagitis
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