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dc.contributor.advisorAtilla, Pergin
dc.contributor.authorTüreli, Serkan
dc.date.accessioned2023-07-18T12:26:41Z
dc.date.issued2023
dc.date.submitted2023-03-15
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dc.identifier.urihttps://hdl.handle.net/11655/33687
dc.description.abstractThe endocannabinoid system, has many functions with its enzymes, ligands and receptors. It’s first discovered receptor is CB1r and the most researched ligand is N-arachidonoylethanolamine (AEA). One of the enzymes involved in the synthesis of AEA is N-acyl-phosphatidylethanolamine-hydrolyzed phospholipase D (PLD), and fatty acid amide hydrolase (FAAH) is one of the enzymes involved in its degradation. The endocannabinoid system regulates the inflammatory processes in the skin and the differentiation, apoptosis and proliferation of keratinocytes in the epidermis. Because of these functions this system is a potential target in inflammatory skin diseases with hyperkeratosis. So we aimed to investigate the effect of the endocannabinoid system in psoriasis, cutaneous lupus erythematosus (CLE) and lichen sclerosis (LS) and compare the synthesis and degradation enzymes of AEA, phospholipase D and FAAH, and CB1r with healthy skin. A prospective, simple randomized, observational study with control group was made. CB1r, FAAH and PLD reactivity and localization in the epidermis were analyzed immunohistochemically and compared with the control group. TNF-α levels as an inflammation marker were measured by ELISA. Immunoreactivity and distribution of CB1r, FAAH ve PLD were different in disease and control groups. In this study, for the first time it is shown that that the loss of CB1r has an effect on the elongation of the rete ridges, which is a typical finding of psoriasis, and in the pathophysiology of CLE and LS, endocannabinoid system defect is present.tr_TR
dc.language.isoturtr_TR
dc.publisherTıp Fakültesitr_TR
dc.rightsinfo:eu-repo/semantics/closedAccesstr_TR
dc.subjectEndokannabinoid sistemitr_TR
dc.subjectPsöriasistr_TR
dc.subjectKutanöz Lupus Eritematozustr_TR
dc.subjectLiken Skleroztr_TR
dc.subjectHiperkeratoztr_TR
dc.subject.lcshDermatolojitr_TR
dc.titlePsöriasis, Kutanöz Lupus Eritematozus ve Liken Skleroz Histopatolojilerinde Kannabinoid 1 Reseptörü (CB1) ve N-Arachidonoylethanolamine (AEA)’nın Yapım ve Yıkım Enzimlerinin Varlığının Araştırılmasıtr_TR
dc.typeinfo:eu-repo/semantics/doctoralThesistr_TR
dc.description.ozetEnzimleri, ligandları ve reseptörleri ile birçok görevi olan endokannabinoid sistemine ait ilk keşfedilen reseptör CB1r, en çok çalışılan ligand ise N- arakidonoiletanolamin (AEA)’dir. N-açil-fosfatidiletanolamin-hidrolize fosfolipaz D (PLD) AEA’nın yapımında, yağ asidi amid hidrolaz (FAAH) ise yıkımında görev alan enzimlerden birisidir. Endokannabinoid sistemi deride inflamatuvar süreçleri yönetir; epidermiste keratinosit farklanmasını, apoptozunu, proliferasyonunu düzenler. Bu görevlerinden dolayı hiperkeratoz ile giden inflamatuvar deri hastalıklarında potansiyel bir hedef olduğu düşünülerek çalışmamızda; psöriasis, kutanöz lupus eritematozus (KLE) ve liken sklerozda (LS) endokannabinoid sisteminin etkisinin araştırılması ve endokannabinoid sistemi reseptörü CB1 ve ligandı AEA’nın yapım ve yıkım enzimleri olan fosfolipaz D ve FAAH’ın sağlıklı deri ile karşılaştırılması amaçlandı. Prospektif, basit randomize, kontrol grubu içeren gözlemsel bir çalışma gerçekleştirildi. CB1r, FAAH ve PLD reaktiviteleri ve epidermisteki lokalizasyonları immünhistokimyasal olarak incelenerek kontrol grubu ile karşılaştırıldı. İnflamasyon belirteci olarak TNF-α düzeyleri ELISA ile ölçüldü. Hastalık gruplarındaki CB1r, FAAH ve PLD dağılımının ve immün reaktivitesinin kontrol grubuna göre farklılık gösterdiği saptandı. Bu çalışma ile psöriasisin tipik bulgusu olan rete kenarlarının uzamasında CB1r’nin kaybının etkisi olduğu ve KLE ile LS patofizyolojilerinde endokannabinoid sistemi bozukluğu olduğu ilk defa gösterildi.tr_TR
dc.contributor.departmentHistoloji ve Embriyolojitr_TR
dc.embargo.terms6 aytr_TR
dc.embargo.lift2024-01-20T12:26:41Z
dc.fundingBilimsel Araştırma Projeleri KBtr_TR
dc.subtypemedicineThesistr_TR


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