当前位置:主页 > 医学论文 > 眼科论文 >

PPAR-γ在慢性鼻-鼻窦炎不伴鼻息肉鼻窦黏膜中的表达及意义

发布时间:2018-03-01 10:47

  本文关键词: 慢性鼻-鼻窦炎 鼻息肉 PPAR-γ 出处:《华中科技大学》2011年硕士论文 论文类型:学位论文


【摘要】:目的:探讨过氧化物酶体增殖物激活物受体-γ(PPAR-γ)在CRSsNP鼻窦黏膜中的表达及临床意义。 方法:应用免疫组织化学技术(immunohistochemistry)和RT-PCR(real time Polymerase chain reaction),检测PPAR-γ在CRSsNP鼻窦黏膜、鼻息肉及正常下鼻甲的表达情况,并分析其差异。 结果:①PPAR-γ在CRSsNP鼻窦黏膜、鼻息肉及正常下鼻甲中均有表达。②PPAR-γ在CRSsNP鼻窦黏膜及鼻息肉中表达比正常下鼻甲组织下降,差别均具有统计学意义(P0.05)。③PPAR-γ在CRSsNP鼻窦黏膜和鼻息肉中的表达无显著性差异。 结论:PPAR-γ在人的鼻腔黏膜中有表达,同时在CRSsNP鼻窦黏膜及鼻息肉中表达下降。PPAR-γ可能与CRSsNP及鼻息肉导致的炎症长期存在有关,提示激活PPAR-γ可能为慢性鼻-鼻窦炎及鼻息肉的治疗提供一种新的方法。
[Abstract]:Aim: to investigate the expression and clinical significance of peroxisome proliferator activator receptor- 纬 (PPAR- 纬) in CRSsNP nasal mucosa. Methods: immunohistochemical technique was used to detect the expression of PPAR- 纬 in CRSsNP sinus mucosa, nasal polyp and normal inferior turbinate by immunohistochemistry and RT-PCR(real time Polymerase chain reaction.At the same time, the difference of PPAR- 纬 expression in CRSsNP nasal mucosa, nasal polyp and normal inferior turbinate was analyzed. Results the expression of PPAR- 纬 in CRSsNP sinus mucosa, nasal polyp and normal inferior turbinate was decreased in CRSsNP sinus mucosa and nasal polyp than in normal inferior turbinate tissue. There was no significant difference in the expression of P0.05. 3PPAR- 纬 in CRSsNP nasal sinus mucosa and nasal polyp. Conclusion the expression of PPAR- 纬 in human nasal mucosa was found in human nasal mucosa, and the decreased expression of PPAR- 纬 in nasal mucosa and nasal polyps of CRSsNP may be related to the long term inflammation induced by CRSsNP and nasal polyps. It suggests that activation of PPAR- 纬 may provide a new method for the treatment of chronic rhinosinusitis and nasal polyps.
【学位授予单位】:华中科技大学
【学位级别】:硕士
【学位授予年份】:2011
【分类号】:R765.41

【参考文献】

相关期刊论文 前1条

1 潘姝;李叶扬;戴丽冰;黄粤;;PPAR-γ在增生性瘢痕成纤维细胞中的表达及意义[J];广东医学;2009年11期



本文编号:1551606

资料下载
论文发表

本文链接:https://www.wllwen.com/yixuelunwen/yank/1551606.html


Copyright(c)文论论文网All Rights Reserved | 网站地图 |

版权申明:资料由用户2c277***提供,本站仅收录摘要或目录,作者需要删除请E-mail邮箱bigeng88@qq.com