银屑病和湿疹患者体内花生四烯酸代谢产物水平检测
发布时间:2018-05-17 05:23
本文选题:银屑病 + 湿疹 ; 参考:《山东大学》2011年硕士论文
【摘要】:研究背景: 1.花生四烯酸(Arachidonic acid, AA)是人体内必需脂肪酸,近年来,AA及其代谢产物在疾病发病中的作用日益受到重视。AA主要通过环氧化酶(Cycloxygenase, COX)和脂氧合酶(Lipoxygenase, LO)途径代谢,白三烯(Leukotrienes, LTs)是人体内花生四烯酸5-脂氧合酶途径的代谢产物,是一种重要的炎症介质,参与疾病的炎症反应。银屑病(Psoriasis, Ps)是一种皮肤科常见病,病因复杂,其发病机制一直是研究的热点。研究表明正常皮肤局部注射LTB4可产生银屑病样皮肤损害,白三烯及其受体在银屑病患者体内异常表达,提示白三烯在银屑病患者体内代谢异常。但是白三烯如何参与银屑病的发病目前尚无研究,白三烯是否参与银屑病的炎症反应需要我们进一步证实。 2.查阅大量文献发现,虽然花生四烯酸在银屑病和湿疹(Eczema, Ec)患者体内均有代谢异常,但在临床研究中,抗白三烯药物和抑制前列腺素合成的药物在湿疹治疗中取得了较好疗效,而抗白三烯药物在银屑病治疗中疗效尚不明确,甚至有报道抑制前列腺素合成药物会加重银屑病患者病情,钟华等的研究表明半胱胺酰白三烯受体虽然在二者皮损中表达均增强,但在银屑病患者中的表达明显强于湿疹患者组,提示AA代谢产物在二者发病中可能有不同机理,需要我们进一步证实。 研究目的: 1.探讨白三烯(LTs)与炎症的关系及在银屑病发病中的作用。 2.比较花生四烯酸(AA)在银屑病(Ps)和湿疹(Ec)患者体内代谢特点异同。 研究方法: 1.采用酶联免疫吸附方法(Enzyme-Linked Immunosorbent Assay, ELISA)分别检测32例银屑病患者血清、尿液和皮损中LTB4、LTE4水平及血清、皮损中IL-8、TNF-α水平,并与20例整形外科健康人员作对照。 2.采用ELISA方法分别检测30例银屑病患者(包括进行期、静止期和退行期Ps患者各10例)、30例湿疹患者(包括急性、亚急性和慢性Ec患者各10例)皮损和10例对照者正常皮肤中LTB4、LTE4、TXB2、6-k-PGFla和PGE2水平。 结果: 1.银屑病患者血清、皮损中IL-8、TNF-α和血清、尿液、皮损中LTE4水平均明显高于对照组(均为P0.01),皮损中LTB4水平明显升高(P0.01),但血清和尿液中LTB4水平与对照组相比差异无显著性(P0.05)。皮损中LTB4、LTE4和IL-8水平与PASI评分变化趋势一致,均有显著相关性。皮损IL-8、TNF-α与LTB4变化趋势一致,均有显著相关性。 2.Ps患者LTB4、LTE4水平进行期组静止期组退行期组对照组。进行期Ps患者组TXB2水平轻度升高(P0.05),6-k-PGFlα、PGE2水平在Ps患者3组中均无明显升高。Ec患者LTE4、PGE2水平急性组亚急性组慢性组对照组,急性和亚急性Ec患者组LTB4、TXB2、6-k-PGF1α水平高于对照组,慢性Ec患者组LTB4、TXB2、6-k-PGF1α水平与对照组相比差异无显著性。 结论: 1.白三烯通过参与局部炎症反应在银屑病发病中起重要作用。 2.Ps患者AA代谢紊乱以5-脂氧合酶(5-LO)途径为主,Ec患者AA代谢5-脂氧合酶途径和环氧化酶(COX)途径均明显增强。
[Abstract]:Research background:
1. Arachidonic acid (AA) is essential fatty acids in the human body. In recent years, the role of AA and its metabolites in the pathogenesis of the disease has been paid more attention to.AA mainly through the pathway of Cycloxygenase (COX) and lipoxygenase (Lipoxygenase, LO), and leukotrienes (Leukotrienes, LTs) are the lipoxygenes of the human peanut four arachidic acid. The metabolites of the synthase pathway, an important inflammatory mediator, participate in the inflammatory response of the disease. Psoriasis (Ps) is a common disease in the Department of dermatology. The etiology is complex and its pathogenesis has always been a hot spot. The study shows that local injection of LTB4 in normal skin can produce psoriatic skin damage, and leukotrienes and their receptors are in psoriasis. The abnormal expression in the patient's body suggests that leukotrienes have abnormal metabolism in the patients with psoriasis, but how leukotrienes are involved in the pathogenesis of psoriasis has not yet been studied. It is necessary to further confirm whether leukotrienes are involved in the inflammatory reaction of psoriasis.
2. a large number of literature found that although peanut four eNIC acid has metabolic abnormalities in patients with psoriasis and Eczema (Ec), in clinical studies, anti leukotrienes and prostaglandin synthetic drugs have achieved good efficacy in the treatment of eczema, and the efficacy of anti leukoenes in the treatment of psoriasis is not clear, even in the treatment of psoriasis. It is reported that inhibition of prostaglandin synthesis can aggravate the condition of patients with psoriasis. Zhong Hua and other studies have shown that although the expression of cysteamine receptor in the two skin lesions is enhanced, the expression in patients with psoriasis is stronger than that of the eczema patients, suggesting that the AA metabolites may have different mechanisms in the two cases, and we need to go in. Step by step.
The purpose of the study is:
1. to explore the relationship between leukotriene (LTs) and inflammation and the role of leukotriene in the pathogenesis of psoriasis.
2. to compare the metabolic characteristics of peanut four enoic acid (AA) in patients with psoriasis (Ps) and eczema (Ec).
Research methods:
1. Enzyme-Linked Immunosorbent Assay (ELISA) was used to detect the serum, urine and skin lesions of 32 patients with psoriasis, the level of LTB4, LTE4 and serum, and the level of IL-8, TNF- a in skin lesions, and compared with 20 cases of plastic surgery health.
2. the ELISA method was used to detect 30 cases of psoriasis (including 10 cases in the stage of progression, static period and degenerative Ps), 30 cases of eczema (including 10 cases of acute, subacute and chronic Ec) and 10 cases of normal skin, LTB4, LTE4, TXB2,6-k-PGFla and PGE2.
Result锛,
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