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Colon cancer is one of the most common cancers observed in men and women in the world, today in many countries after cardiovascular diseases; it is second leading cause of death. In this the study we aimed to investigate the effects of use of Cucurbitacin I and together with Geldanamycin (GA) which have apoptotic and anti-proliferativeeffects on HT29. Cells were treated with GA, CU and GA+CU. Effect of GA, CU on cell viabilitywere demonstrated by MTT assay and activities of bax, caspase-3, bcl-2, GRP78, wee1, AIF and GAAD153 were performedwith ELISA method after 48 hour treatment. Our study showed that the combined use of GA and CU significantly reduced cell viability of colon cells. Also, the same dose of GA and CU used together increased the expression of proapoptotic proteins and decreased anti-apoptotic proteins more than their effects alone. As aconclusion, our study showed that GA and CU synergistically induce apoptosis on humancolon cancer.

Objective: We aimed to research that naringin whether protects from renal ischemia/reperfusion induced renal damage in rats. Methods: Twenty-four Wistar albino female rats randomly were divided into three groups: 1) control group, in which the rats were only performed right nephrectomy; 2) a second group received right nephrectomy and left kidney ischemia (1 h) and reperfusion (24 h) group ischemia/reperfusion (I/R); 3) a third group received 50 mg/kg naringin orally once a day for two weeks before ischemia/reperfusion (I/R/N). Expression of cyclooxygenase-2 (COX-2), cytosolic phospholipase A2 (cPLA2), inducible nitric oxide synthase (iNOS), caspase-3, B-cell lymphoma-2 (Bcl-2), Bcl-2 associated x protein (Bax), serum creatinine (Cr), tumor necrosis factor α (TNF-α), interleukin 6 (IL-6) were measured by using enzyme-linked immunosorbent assay (ELISA). Results: Naringin-treated rats that performed renal ischemia/reperfusion demonstrated significant decrease in Cr, IL-6 and TNF-α levels when compared to the only renal ischemia/reperfusion performed rats. While renal ischemia/reperfusion caused a decrease of bcl-2 (1.72 ± 0.20 pg/ml) levels, while an increase of COX-2 (11882 ± 642 pg/ml), cPLA2 (2448 ± 139 pg/ml), iNOS (4331 ± 438 IU/ml), cleaved caspase-3 (7.33 ± 0.76 ng/ml) and Bax (2.33 ± 0.44 ng/ml) levels. The treatment of naringin reversed these kidney effects (7.47 ± 60.35 pg/ml; 9299 ± 327 pg/ml; 2001 ± 78 pg/ml; 3112 ± 220 IU/ml; 3.38 ± 0.54 ng/ml; 2.33 ± 0.44 ng/ml, respectively) (p

Apoptotic pathways are important for resistance to chemotherapeutics drugs and cancer development. Metformin is a safe, inexpensive and effective drug used to treat type 2 diabetes. Furthermore, although there is evidence of anticancer effects, the mechanisms by which metformin exerts the effects are unclear. Therefore, it was aimed to investigate Bcl-2, kaspaz-3, bax, wee-1, AIF, grp78 and gadd153 levels in metformin treated skin cancer cells. Materials and Methods: The skin cancer cells (B16F10) were treated with metformin and kaspase-3, bcl-2, wee 1, gadd153, grp78 and AIF levels were analyzed by using ELISA. Result: Treatment of metformin increased of proapoptotic proteins (kaspase-3, bcl-2, wee 1, gadd153, grp78 and AIF) and decreased antiapoptotic protein (bcl2). Conclusion: In conclusion, this study showed that metformin has apoptotic effect on melanoma skin cancer. Kanserlerde kemoterapötiklere gösterilen dirençte ve kanser gelişiminde apoptozisin önemli rolü vardır. Metformin tip 2 diyabet tedavisinde kullanılan güvenli, ucuz ve etkili bir ilaçtır. Ayrıca, antikanser etkilerinin olduğuna dair kanıtlar olmasına rağmen metforminin bu etkiyi hangi mekanizmalar ile gerçekleştirdiği açık değildir. Bu nedenle, bu çalışmada metformin cilt kanseri hücrelerinde Bcl-2, caspaz-3, bax, wee-1, AIF, grp78 ve gadd153 düzeyleri üzerine etkileri araştırıldı. Gereç ve Yöntem: Deri kanseri hücrelerine (B16F10) metformin uygulandı ve kaspaz-3, bcl-2, hafta 1, gadd153, grp78 ve AIF seviyeleri ELISA kullanılarak ölçüldü. Bulgular: Çalışmamızda metforminin cilt kanseri hücrelerinde apoptozis proteinlerini (caspaz-3, wee 1, gadd153, grp78 ve AIF) arttırdığı ve antiapoptotik markırı (bcl-2) azalttığı belirlendi. Sonuç: Çalışma sonuçları metforminin melanom cilt kanseri üzerine apoptotik etkisinin olduğunu gösterdi.

WOS: 000452553400008 Background and Objective: Hypericum perforatum, which have various names locally such as St. John Wort, is a plant which blooms between July and September at farms, borders of roads and woods, top of hills and grasslands, which is regulator of apoptotic mediators are shown in various studies. Also, it is known that gentamicin activates apoptotic mediators and causes necrosis in kidney. Due to this reason, a study was planned to examine the protective effects of Hypericum perforatum on nephrotoxicity caused by gentamicin. Materials and Methods: Mice were divided into three groups; control group, gentamicin group and perforatum extract group. About 100 mg kg(-1 )gentamicin and 70 mg kg(-1) H. perforatum extract are administered to related groups for 9 days. Renal tissue samples and blood samples are obtained for biochemical analysis. caspase-3, bax and bcl-2 proteins are analyzed by using ELISA method. Results: Gentamicin administration increased caspase-3, bax while it decreased bcl-2. H. perforatum administration to mice that are administered gentamicin previously decreased the rate of caspase-3, bax caused by gentamicin while it increased bcl-2. Gentamicin also increased serum BUN, creatinine, TOS and TNF-alpha levels and renal MDA levels significantly and decreased catalase (CAT) and glutathione (GSH) significantly compared to other groups. Gentamicin+perforatum extract treatment reversed these factors compared to the gentamicin group (p

WOS: 000396710600003 Objective: Hypericum perforatum, which have various names locally such as "sari kantaron, kanotu, kilicotu, mayasilotu, yaraotu", is a plant which blooms between july and september at farms, borders of roads and woods, top of hills and grasslands, whose anti-inflammatory and antioxidant effects are shown in various studies. Due to this reason, we planned a study to examine the protective effects of Hypericum perforatum on ototoxicity caused by gentamicin. Methods: For this purpose, 100 mg/kg gentamicin and 70 mg/kg Hypericum perforatum extract are administered to mice for 9 days. On the 9th and 10th days rotarod performance was assessed to evaluate the Gentamicin and Hypericum Perforatum extract on motor coordination of mice. Results: Gentamicine treatment decreased fall latency of mice and Gentamicine together Hypericum Perforatum extract treatment increased fall latency of mice. Conclusion: Our study showed that Hypericum Perforatum extract will be usefull to prevent gentamicin induced ototoxicity

Amaç: İzole fare gastrik fundus striplerinde etanol (164 mM) ile indüklenen kontraksiyonlarda fosfolipaz C, protein kinaz C ve endotelin dönüştürücü ezimin muhtemel rolünü araştırmak. Yöntem ve gereç: Fareler öldürüldükten sonra mide izole edildi ve longitudinal kas stripleri gastrik fundustan hazırlandı. Stripler organ banyosuna asıldı ve cevaplar izometrik olarak kaydedildi. Etanol (164 mM) organ banyolarına uygulandı ve stabil kontraksiyon cevabı elde edildi. İlk etanol cevabı kaydedildikten sonra, preparatlar ayrı ayrı olarak lidokain (1- 100 ?M), neomisin (10-500 ?M), safingol (0.5-5 ?M) ve SM-19712 (1-50 ?M) ile 40 dakika boyunca inkübe edildi. Daha sonra aynı kimyasal ajan varlığında ikinci etanol cevabı elde edildi. Bulgular: Lidokain (1-100 ?M) (lokal anestezik ajan) izole fare gastrik fundal striplerinde etanol ile indüklenen kontraksiyonları modüle etmedi. Bunun zıttında, neomisin (10-500 ?M) (fosfolipaz C’nin selektif inhibitörü) ve safi ngol (0.5-5 ?M) (protein kinaz C’nin selektif inhibitörü) etanol ile indüklenen kontraksiyonları azalttı. Bununla birlikte, SM- 19712 (1-50 ?M) (endotelin dönüştürücü enzimin selektif inhibitörü) bu kontraksiyonları etkilemedi. Sonuç: Fare gastrik fundal striplerinde etanolün kontraktil cevapları nöronal olmaktan çok müsküler olabilir. Buna ilave olarak, fare gastrik fundusunda etanole bağlı olan kontraksiyonlarda fosfolipaz C ve protein kinaz C yolaklarının rolü olabilir. Diğer taraftan, aynı dokuda etanolün kontraktil cevaplarında endotelin dönüştürücü enzimin regülatör rolü olmayabilir. Aim: To evaluate the possible roles of phospholipase C, protein kinase C, and endothelin-converting enzyme on contractions induced by ethanol (164 mM) in isolated gastric fundal strips of mice. Materials and methods: Aft er the mice were killed, the stomach of each was removed and longitudinal muscle strips were prepared from the gastric fundus. The strips were mounted in organ baths and their responses were recorded isometrically. Ethanol (164 mM) was added to the organ baths and a steady-state contraction was obtained. After the first ethanol response was recorded, the preparations were incubated separately with lidocaine (1-100 µM), neomycin (10-500 µM), safingol (0.5-5 µM), and SM-19712 (1-50 µM) for 40 min. The second ethanol response was then examined in the presence of the drug used in the incubation period. Results: Lidocaine (1-100 µM), a local anesthetic agent, did not modulate the contractions induced by ethanol in isolated gastric fundal strips of mice. In contrast, neomycin (10-500 µM), a selective inhibitor of phospholipase C, and safi ngol (0.5-5 µM), a selective inhibitor of protein kinase C, decreased the ethanol-induced contractions. SM-19712 (1-50 µM), a selective inhibitor of endothelin-converting enzyme, failed to aff ect these contractions. Conclusion: The contractile effect of ethanol may be muscular rather than neuronal in the gastric fundal strips of mice. In addition, phospholipase C and protein kinase C pathways may have a role in contractions due to ethanol in the mouse gastric fundus. On the other hand, endothelin-converting enzyme may not have a regulatory role in the contractile responses of ethanol in the same tissue.

TEZ6567 Tez (Yüksek Lisans) -- Çukurova Üniversitesi, Adana, 2007. Kaynakça (s.39-43) var. xii, 44 s. ; 29 cm. Bu çalısmada, bir HMG-KoA redüktaz inhibitörü olan rosuvastatinin (30 mg/kg/gün, 30 gün boyunca) kronik olarak uygulamasının fare torasik aorta ve korpus kavernozum (CC) dokularında Rho-kinaz enzim ekspresyonu ve aktivasyonu üzerine olası etkileri hem Western blot analizleri hem de izole organ banyosu deneyleri ile incelendi. 30 günlük uygulama sonrasında rosuvastatin verilen farelerin serum total kolesterol düzeyleri, rosuvastatin verilmeyen farelere göre anlamlı olarak düsüktü. Rosuvastatin verilen farelerden izole edilen aortta bir a1 adrenoseptör agonisti olan fenilefrine verilen kasılma yanıtları degismezken, bu grupta KCl yanıtlarının azaldıgı görüldü. Bu farelerin CC'larında rosuvastatin uygulaması fenilefrine ait EC50 degerini arttırdı. Rosuvastatin alan gruptan izole edilen hem aorta hem CC dokularında Rho-kinaz enziminin selektif inhibitörü olan Y- 27632'ye verilen gevseme yanıtları kontrole göre anlamlı bir sekilde arttı. Bununla birlikte rosuvastatin alan farelerin torasik aorta ve CC dokularında Rho-kinaz enzim ekspresyonu veya aktivasyon düzeyleri kontrole göre farklı degildi. In this study, we investigated the effects of chronic inhibition of HMG-CoA reductase with rosuvastatin intake (30 mg/kg/day, via gastric gavage, 30 days) on Rho-kinase enzyme expression and activation by Western blot analysis and isolated organ bath experiments on the thoracic aorta and corpus cavernosum(CC) in the mice. In the rosuvastatin-treated mice, serum total cholesterol level was significantly lower than the untreated mice. Contractile responses of the aorta obtained from rosuvastatin-treated mice to a1-adrenoceptor agonist phenylephrine were not changed while KCl-induced contractions were decreased when compared to those of untreated group. Contractile responses of the CC obtained from rosuvastatin-treated group to phenylephrine were not changed while EC50 for phenylephrine was significantly increased. Relaxant responses to Rho-kinase inhibitor Y-27632 were significantly increased in both thoracic aorta and CC obtained from rosuvastatin-treated mice. In western blot analysis, expression and activation levels in rho-kinase were not different in the aorta and CC from mice treated with rosuvastatin when compared to those of untreated mice Bu çalışma Ç.Ü. Bilimsel Araştırma Projeleri Birimi Tarafından Desteklenmiştir. Proje No:TF2006YL3

Bu çalısmada, bir HMG-KoA redüktaz inhibitörü olan rosuvastatinin (30mg/kg/gün, 30 gün boyunca) kronik olarak uygulamasının fare torasik aorta vekorpus kavernozum (CC) dokularında Rho-kinaz enzim ekspresyonu veaktivasyonu üzerine olası etkileri hem Western blot analizleri hem de izole organbanyosu deneyleri ile incelendi. 30 günlük uygulama sonrasında rosuvastatinverilen farelerin serum total kolesterol düzeyleri, rosuvastatin verilmeyen fareleregöre anlamlı olarak düsüktü.Rosuvastatin verilen farelerden izole edilen aortta bir 1 adrenoseptöragonisti olan fenilefrine verilen kasılma yanıtları degismezken, bu grupta KClyanıtlarının azaldıgı görüldü. Bu farelerin CC'larında rosuvastatin uygulamasıfenilefrine ait EC50 degerini arttırdı. Rosuvastatin alan gruptan izole edilen hemaorta hem CC dokularında Rho-kinaz enziminin selektif inhibitörü olan Y-27632'ye verilen gevseme yanıtları kontrole göre anlamlı bir sekilde arttı. Bununlabirlikte rosuvastatin alan farelerin torasik aorta ve CC dokularında Rho-kinazenzim ekspresyonu veya aktivasyon düzeyleri kontrole göre farklı degildi.Çalısmamızın sonuçları, farelerde rosuvastatin uygulamasıyla HMG-KoAredüktaz enziminin kronik inhibisyonunun bu hayvanlardan izole edilen korpuskavernozum dokusunda, fenilefrine verilen kasılma yanıtlarında bir baskılanmayave torasik aortasında KCl'ye verilen kasılma yanıtlarında bir azalmaya nedenoldugunu ve bu uygulamanın her iki dokuda Rho-kinaz enziminin selektifinhibitörü olan Y-27632'ye verilen gevseme yanıtlarını arttırdıgını göstermektedir. In this study, we investigated the effects of chronic inhibition of HMG-CoAreductase with rosuvastatin intake (30 mg/kg/day, via gastric gavage, 30 days) onRho-kinase enzyme expression and activation by Western blot analysis andisolated organ bath experiments on the thoracic aorta and corpus cavernosum(CC)in the mice. In the rosuvastatin-treated mice, serum total cholesterol level wassignificantly lower than the untreated mice.Contractile responses of the aorta obtained from rosuvastatin-treated miceto 1-adrenoceptor agonist phenylephrine were not changed while KCl-inducedcontractions were decreased when compared to those of untreated group.Contractile responses of the CC obtained from rosuvastatin-treated group tophenylephrine were not changed while EC50 for phenylephrine was significantlyincreased. Relaxant responses to Rho-kinase inhibitor Y-27632 were significantlyincreased in both thoracic aorta and CC obtained from rosuvastatin-treated mice.In western blot analysis, expression and activation levels in rho-kinase were notdifferent in the aorta and CC from mice treated with rosuvastatin when comparedto those of untreated mice.These findings suggest that chronic inhibition of HMG-CoA reductase byrosuvastatin not only leads to decrease in the contractile responses to KCl in thethoracic aorta and to phenylephrine in the CC but also increase in the relaxant 56