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MEZENKİMAL KÖK HÜCRELERİN RATLARDA CROHN HASTALIĞI MODELİNDE DOKU HASARI, İNFLAMATUAR VE ANTİNFLAMATUAR SİTOKİNLERE ETKİSİ

EFFECTS OF MESENCHYMAL STEM CELLS ON TISSUE INJURY, INFLAMMATORY AND ANTI-INFLAMMATORY CYTOKINES IN CROHN’S DISEASE MODEL IN RATS

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Abstract (2. Language): 
Background: Mesenchymal stem cells (MSC) have immune supressive effects by decreasing inflammatory cytokines (IFN-γ, TNF-α) increasing antiinflammatory cytokines (IL-10) and inhibiting T cells and antigen presenting cells. Various cytokines are responsible for mucosal damage in Crohn‘s disease and TNF-α is one of the most important of them. The aim of this study is to determine the role of MSC in the treatment of Crohn‘s disease model. Methods: 3% Dextran sulphate sodium (DSS) is used to make Crohn‘s disease model. There are 7 groups which composed of 6 rats in each group; Group 1: SHAM group, Group 2: DSS+ placebo, Group 3: DSS+ methylprednisolone 1 mg/kg, po, Group 4: DSS + mesalazine 100 mg/kg, po., Group 5: DSS+ MKH, 106 cell/rat, intraperitoneal, Group 6: DSS + methylprednisolone 1 mg/kg, po + MSC, 106 cell/rat, intraperitoneal, Group 7: DSS + mesalazine 100 mg/kg, po + MSC, 106 cell/rat, intraperitoneal. Groups are compared with the alteration of pathological and biochemical (TNF, INF IL-10) parameters. Results: The average scores of group 1, 2 and 3 were higher than the average scores of Group 5, 6 and 7 significantly in pathological evaluation (p<0.05). IL-10 was 108.33±2.23 pg/ml in Group 1, 80.83±3.62 pg/ml in Group 2 where the levels of IL-10 were 131.66±3.83 pg/ml, 138.33±3.19 pg/ml and 115.33±5.21 pg/ml in Group 5, 6 and 7 respectively, in which MSC was used as a treatment. It is observed that the average of these three groups were significantly higher (p<0.05). Conclusion: This study suggest that MSC may take a role in the treatment of Crohn‘s disease by increasing the amount of IL-10.
Abstract (Original Language): 
Amaç: Mezenkimal kök hücreler (MKH) T hücre oluĢumunu ve antijen sunan hücreleri inhibe ederek inflamatuar sitokinlerin salınımını baskılayarak (IFN-γ, TNF-α) ve antiinflamatuar sitokinlerin (IL-10) salınımını arttırarak immunsupresiv etki oluĢturmaktadırlar. Crohn hastalığında bağırsaklarda oluĢan mukozal hasarda ise birçok sitokin sorumlu olmakla birlikte TNF-α bunlar içerisinde önde gelenlerdendir. Bu çalıĢmanın amacı MKH lerin Deneysel Kolit modelinde tedavideki yerini belirlemektir. Gereç ve yöntem: Deneysel kolit oluĢturmak için %3 Dekstran sülfat sodyum (DSS) kulllanıldı. ÇalıĢma her grup da 6 sar rat olmak üzere 7 grup üzerinde yapıldı: Grup 1:SHAM grubu, Grup 2: DSS+ placebo, Grup 3: DSS+ metilprednisolon 1 mg/kg, po, Grup 4: DSS + mesalazin 100 mg/kg, po., Grup 5: DSS+ MKH,106 hücre/rat, intraperitoneal, Grup 6: DSS + metilprednisolon 1 mg/kg, po + MKH,106 hücre/rat, intraperitoneal, Grup 7: DSS + mesalazin 100 mg/kg, po + MKH, 106 hücre/rat, intraperitoneal. Gruplar patolojik ve biyokimyasal (TNF, INF IL-10) parametrelerdeki değiĢimler ölçülerek karĢılaĢtırıldı. Bulgular: Patolojik değerlendirmede Grup 1, 2 ve 3‘ün ortalama skorlarının Grup 5, 6 ve 7‘nin ortalama skorlarından belirgin yüksek olduğu gözlendi (p<0,05). IL-10 düzeyi Grup 1 için 108,33±2,23 pg/ml, Grup 2 için 80,83±3,62 pg/ml olup MKH tedavisi verilen gruplar olan Grup 5, 6 ve 7 de bu değerler sırasıyla 131,66±3,83 pg/ml, 138,33±3,19 pg/ml ve 115,33±5,21 pg/ml olarak ölçülmüĢ olup, bu son üç grup ortalamalarının anlamlı olarak yüksek olduğu gözlendi (p<0,05). IFN-γ ve TNF-α düzeyleri açısından gruplar arasında anlamlı bir fark bulunmadı. Sonuç: Bu çalıĢmanın sonucuna göre MKH‘in IL-10 düzeyini yükselterek Crohn hastalığı tedavisinde yeri olabileceği düĢünülebilir
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