Çinkodan zengin diyetin, sigara dumanı maruziyetindeki sıçan mesane dokusu sitokin profiline etkisi
Küçük Resim Yok
Tarih
2015
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Dergi ISSN
Cilt Başlığı
Yayıncı
Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Amaç: Sigara içimi akciğer, larinks, özefagus, mide, mes ane ve böbrek kanserleri ile kronik hastalıkların sebebidir. Sitokinler, inflamasyonun başlatılması ve sürdürülmesinde önemlidirler. Sigara, çinko eksikliği sebebidir. Çinko, antioksidan olup serbest radikallerin zararlarından hücreleri korur. Çalışmamızda sigara dumanına maruz bırakılarak çinkodan zengin diyet ile beslenen sıçanların mesane dokusundaki TLR 2, TLR 4, Nükleer faktör ka ppa B, İnterl ökin 1? ve İnterlökin 10 ekspresyonuna etkisi incelenmesi amaçlanmıştır. Yöntem : Çalışmada 24 adet erişkin erkek Wistar-Albino sıçanlar kullanıldı. Sıçanlar 4 gruba ayrıldı. Birinci grup normal, 2. grup ise çinkodan zengin diyetle beslendi. Üçüncü ve 4. gruplar sigara inhalasyonu yapılan gruplar olup sırasıyla normal ve çinkodan zengin diyetle beslenen gruplardı. Den ey sonunda alınan mesane dokuları histol ojik olarak değerlendirildi. Kalan doku örnekleri ise Real time polymerase chain reaction yöntemi ile sitokin ekspresyonları gösterilerek değerlendirildi. Bulgular: Çalışmadaki hiçbir grup mesane epitelinde değ işikli k izlenmemiştir. Sigara verilen grupta sadece düz kas yapılarında tabakalar arasında ödem ve bazı alanlarda yoğun inflamatuar hücreler ile bu alanlarda hemoraji ve konjesyona rastlanılmıştır. Çinkodan zengin diyetle besl enen denekler de ise inflamatuar hüc relere, konjesyona ve ödeme daha az rastlandı. Tüm sıçan gruplarının mesane dokularında sitokin ekspresyonları ikili olarak karşılaştı rmalarda sigaraya maruz kalmış sıçanlarda çinko almayan ve çinko alan sıçanlar için NF -?B2 geni için anlamlı farklılık bul undu. Sonuç : Sonuç olarak sigara maruz kalan sıçanlarda çinko kullanımının anlamı bir şekilde NF -?B2 ekpresyonunu artışına neden olması, çinkonun sigaraya bağlı gelişen mesane kanserlerinde kanserli hücre apopitozunu arttırarak tedaviye katkı yapabileceğin i düşündürmektedir.
Objective : Cigarette smoking causes lung, larynx, esoph agus, stomach, bladder and kidney cancers and chronic diseases. Cytokines are important in initiating and mai ntai n ing inflammation. Smoking is the cause of zinc deficie ncy. Zinc i s an antioxidant and protects cells from free radical damage. In our study, it was aimed to investigate the effect of cigarette smoke exposure on expression of Toll -like receptor 2, Toll -like receptor 4, nuclear factor kappa B, interleukin 1β and interleukin 10 in the bladder tissue of rats fed with zinc rich diet. Method : In this study 24 adult male Wistar-Albino rats were used. The rats were divided into 4 groups. First group was fed with normal diet, the 2nd group was fed with zinc rich diet. Third and 4th groups were exposed to cigarette inhalation and fed with normal and zinc rich diet respe ctive ly. The bladder tissues were taken at the end of the experiment and evaluated histologically. The remaini ng tissue samples were evaluated by the method of Real time polymerase chain reaction to show cytokine expression. Results : No changes in urinary bladder epithelium was observed in all study groups. Edema and inflammatory cells in the smooth muscle layers with intense hemorrhage and congestion were observed in cigarette smoke given group. Less inflammatory cells, congestion and edema have been found in the rats fed with zinc rich diet. Cytokine expression in bladder tissue of all groups of rats compared in pairs and significant difference was found for the NF -κb2 gene in zinc rich supplemented and normally supplemented rats e x- posed to cigarette smoke. Conclusion : As a result, a significant increase in expression of NF -κb2 caused by the use of zinc in rats ex posed to cigarette smoke suggests that zinc can contribute the treatment of bladder cancer due to smoking by increasing cancer cell.
Objective : Cigarette smoking causes lung, larynx, esoph agus, stomach, bladder and kidney cancers and chronic diseases. Cytokines are important in initiating and mai ntai n ing inflammation. Smoking is the cause of zinc deficie ncy. Zinc i s an antioxidant and protects cells from free radical damage. In our study, it was aimed to investigate the effect of cigarette smoke exposure on expression of Toll -like receptor 2, Toll -like receptor 4, nuclear factor kappa B, interleukin 1β and interleukin 10 in the bladder tissue of rats fed with zinc rich diet. Method : In this study 24 adult male Wistar-Albino rats were used. The rats were divided into 4 groups. First group was fed with normal diet, the 2nd group was fed with zinc rich diet. Third and 4th groups were exposed to cigarette inhalation and fed with normal and zinc rich diet respe ctive ly. The bladder tissues were taken at the end of the experiment and evaluated histologically. The remaini ng tissue samples were evaluated by the method of Real time polymerase chain reaction to show cytokine expression. Results : No changes in urinary bladder epithelium was observed in all study groups. Edema and inflammatory cells in the smooth muscle layers with intense hemorrhage and congestion were observed in cigarette smoke given group. Less inflammatory cells, congestion and edema have been found in the rats fed with zinc rich diet. Cytokine expression in bladder tissue of all groups of rats compared in pairs and significant difference was found for the NF -κb2 gene in zinc rich supplemented and normally supplemented rats e x- posed to cigarette smoke. Conclusion : As a result, a significant increase in expression of NF -κb2 caused by the use of zinc in rats ex posed to cigarette smoke suggests that zinc can contribute the treatment of bladder cancer due to smoking by increasing cancer cell.
Açıklama
Anahtar Kelimeler
Genel ve Dahili Tıp, Tıbbi Araştırmalar Deneysel, Üroloji ve Nefroloji
Kaynak
Abant Tıp Dergisi
WoS Q Değeri
Scopus Q Değeri
Cilt
4
Sayı
2
