当前位置:主页 > 医学论文 > 皮肤病论文 >

寻常型银屑病皮损中HBD-2、IL-1β和NF-κBp65表达的研究

发布时间:2018-04-03 13:54

  本文选题:寻常型银屑病 切入点:HBD-2 出处:《山西医科大学》2011年硕士论文


【摘要】:目的:探讨HBD-2、IL-lβ和NF-κBp65在寻常型银屑病皮损中的表达与寻常型银屑病严重程度的关系及其在寻常型银屑病中的作用机制。 方法:1.采用免疫组化法检测45例寻常型银屑病患者皮损组织、45例寻常型银屑病患者非皮损组织及15例正常皮肤组织标本中HBD-2、IL-lβ、NF-κBp65的表达,比较不同组别间三者表达的差异,并对HBD-2、IL-lβ、NF-κBp65进行相关性分析。2.根据PASI评分将45例寻常型银屑病患者分为三组:轻度组25例、中度组12例、重度组8例。检测轻、中、重寻常型银屑病患者皮损区HBD-2、IL-lβ、NF-κBp65的表达,比较不同组别间三者表达的差异,分析三者在寻常型银屑病患者皮损中的相关性。 结果:1.寻常型银屑病患者皮损区HBD-2、IL-lβ、NF-κBp65的表达比寻常型银屑病患者非皮损区、正常人皮肤明显上调,在寻常型银屑病患者非皮损区HBD-2、IL-lβ的表达亦高于正常人皮肤,差异均有统计学意义(均P0.05)。2. HBD-2、IL-lβ、NF-κBp65在寻常型银屑病重度患者皮损区的表达明显高于中度组、轻度组、正常对照组;其在中度患者皮损区的表达高于轻度组及正常对照组,并且轻度组高于正常对照组,差异均具有统计学意义(均P0.05)。3.在轻、中、重寻常型银屑病患者皮损中HBD-2与lL-lβ, HBD-2与NF-KBp65、IL-lβ与NF-κBp65表达水平之间均存在正相关(r=0.869、0.740、0.814,均P0.05)。 结论:1. HBD-2、IL-lβ在正常人皮肤组织、寻常型银屑病非皮损区、寻常型银屑病皮损区中表达呈逐渐上调,提示HBD-2、IL-lβ与寻常型银屑病的发生、发展过程密切相关。2.NF-κB p65在寻常型银屑病皮损区表达上调,提示NF-κB p65与寻常型银屑病发病密切相关。3.本实验结果表明HBD-2、IL-lβ、NF-κB p65在寻常型银屑病皮损中的表达均升高,且三者之间均存在正相关,我们推测三者之间可能存在相互作用共同参与了银屑病的发病过程。
[Abstract]:Objective: to investigate the relationship between the expression of IL-l 尾 and NF- 魏 Bp65 in psoriasis vulgaris and the severity of psoriasis vulgaris.Method 1: 1.The expression of HBD-2mIL-l 尾 -NF- 魏 Bp65 in 45 cases of psoriasis vulgaris and 15 cases of normal skin tissue was detected by immunohistochemical method, and the differences among the three groups were compared.The correlation between IL-1 尾 and NF- 魏 Bp65 of HBD-2 was analyzed.According to PASI score, 45 patients with psoriasis vulgaris were divided into three groups: mild group (25 cases), moderate group (12 cases) and severe group (8 cases).To detect the expression of IL-l 尾 -NF- 魏 Bp65 in lesions of patients with mild, moderate and severe psoriasis, to compare the differences among the three groups, and to analyze the correlation among them in the lesions of patients with psoriasis vulgaris.The result is 1: 1.The expression of IL-l 尾 -NF- 魏 Bp65 in the lesions of psoriasis vulgaris was significantly higher than that in the non-lesions of psoriasis vulgaris and in the normal skin, and the expression of IL-l 尾 in the non-lesions of psoriasis vulgaris was significantly higher than that in the normal skin (all P 0.05. 2).The expression of IL-l 尾 -NF- 魏 Bp65 in severe psoriasis vulgaris was significantly higher than that in moderate group, mild group and normal control group, and was higher in moderate group than in mild group and normal control group, and in mild group was higher than that in normal control group.The difference was statistically significant (all P 0.05. 3).There was a positive correlation between the expressions of HBD-2 and lL-l 尾, HBD-2 and NF-KBp65, IL-l 尾 and NF- 魏 Bp65 in patients with mild, moderate and severe psoriasis vulgaris (P 0.05).Conclusion 1.The expression of IL-l 尾 in normal human skin, psoriasis vulgaris and psoriasis vulgaris was gradually up-regulated, suggesting the occurrence of IL-l 尾 and psoriasis vulgaris.2. The expression of NF- 魏 B p65 in psoriasis vulgaris was up-regulated, suggesting that NF- 魏 B p65 was closely related to the pathogenesis of psoriasis vulgaris.The results showed that the expression of IL-l 尾 -NF- 魏 B p65 in psoriasis vulgaris was increased, and there was a positive correlation among them. We speculate that the interaction among them may be involved in the pathogenesis of psoriasis.
【学位授予单位】:山西医科大学
【学位级别】:硕士
【学位授予年份】:2011
【分类号】:R758.63

【参考文献】

相关期刊论文 前5条

1 王伯瑶,吴崎;内源性抗生素肽──天然免疫的重要介质[J];生命科学;1999年S1期

2 杨琴;甄莉;;白细胞介素-1β对Hacat细胞诱导产生β防御素-2表达的研究[J];中国药物与临床;2008年02期

3 刘玮,赵庆利,Reno Debets,蔡瑞康,Errol P Prens;白介素-1β诱导正常人皮肤表达银屑病免疫病理表型[J];中华皮肤科杂志;1999年02期

4 杨政,文海泉;寻常型银屑病患者皮肤中诱生型一氧化氮合酶、核因子-κBp65表达及其临床意义[J];中华皮肤科杂志;2001年02期

5 Hajime Isomoto;Hiroshi Mukae;Hiroshi Ishimoto;Yoshito Nishi;Akihiro Wada;Ken Ohnita;Toshiya Hirayama;Masamitsu Nakazato;Shigeru Kohno;;High concentrations of human β-defensin 2 in gastric juice of patients with Helicobacter pylori infection[J];World Journal of Gastroenterology;2005年31期



本文编号:1705473

资料下载
论文发表

本文链接:https://www.wllwen.com/yixuelunwen/pifb/1705473.html


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

版权申明:资料由用户30be2***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