ANKAFERD BLOOD STOPPER BAX/BCL-2 VE CYT-C/CAS-3 YOLAKLARI ARACILIĞIYLA MİTOKONDRİYAL STRESLE İLİŞKİLİ APOPTOZU AZALTARAK KADMİYUM KAYNAKLI AKCİĞER HASARINI HAFİFLETİR

Amaç Çevresel faktörlerin bir sonucu olarak vücuda alınan kadmiyum (Kd) akciğer dokularında inflamasyon, oksidatif stres ve artan apoptozis ile hasara neden olur. Hemostatik bir ajan olarak kullanılan Ankaferd Blood Stopper (ABS), bileşimindeki beş farklı bitki özü ve bileşeni nedeniyle antioksidan, antienflamatuar, antibakteriyel, antiapoptotik ve yara iyileştirici özelliklere sahiptir. Bu nedenle çalışmamızda Kd’un akciğer üzerinde oluşturduğu toksisite üzerine ABS’nin iyileştirici etkisini araştırmayı amaçladık. Gereç ve Yöntem Çalışmada 32 rat kullanıldı ve her grupta 8 rat olmak üzere 4 gruba ayrıldı: kontrol, Kd (2,5 mg/kg tek doz ip), ABS (1,5 ml/kg tek doz ip) ve Kd+ABS (Kd, 2,5 mg/kg tek doz ip-ABS, 1,5 ml/kg tek doz ip). Akciğer dokuları histopatolojik olarak değerlendirildi. İnflamasyon, tümör nekroz faktörü-α (TNF-α) ile immünohistokimyasal olarak değerlendirildi. Oksidatif stres, total oksidan seviye (TOS) ve total antioksidan seviye (TAS) ile spektrofotometrik yöntem kullanılarak değerlendirildi. Apopitoz, Bcl-2 ile ilişkili X (Bax), B-hücreli lenfoma 2 (Bcl-2), Sitokrom c (Sit c) ve kaspaz 3 genlerinin rölatif mRNA kat değişimleri ile RT-PCR yöntemi kullanılarak değerlendirildi. Bulgular Kd grubunda, konjesyon, hemoraji ve mononükleer hücre infiltrasyonu gibi histopatolojik bulgularda artış bulundu. Kd’un TNF-α'yı yükselterek inflamasyonu arttırdığı, TOS ve OSİ artırıp TAS'ı azaltarak oksidatif stres artışına neden olduğu ayrıca Bax, Sit c ve kaspaz 3 gen ekspresyonlarının arttırıp Bcl-2 gen ekspresyonunu azaltarak mitokondriyal stres ile ilişkili apoptozise neden olduğu bulundu (p<0.05). ABS uygulamasından sonra tüm bu parametrelerde anlamlı düzelme olduğu belirlendi (p<0.05). Sonuç Sonuç olarak, ABS'nin Kd kaynaklı akciğer toksisitesinden koruyucu alternatif bir seçenek olabileceği ve bu konuda daha fazla araştırma yapılması gerektiği kanısındayız.

ANKAFERD BLOOD STOPPER ALLEVIATES CADMIUM-INDUCED LUNG INJURY BY REDUCING MITOCHONDRIAL STRESS-RELATED APOPTOSIS VIA BAX/BCL-2 AND CYT-C/CAS-3 PATHWAYS

As a result of environmental factors, cadmium (Cd) taken into the body causes damage to lung tissues through inflammation, oxidative stress, and increased apoptosis. Ankaferd Blood Stopper (ABS), which is used as a hemostatic agent, has antioxidant, antiinflammatory, antibacterial, antiapoptotic, and wound healing properties due to five different plant extracts and components in its composition. Therefore, in our study, we aimed to investigate the curative effect of ABS on the toxicity of Cd on the lung. Material and Method Thirty two rats were used in the study, and they were divided into 4 groups, with 8 rats in each group: control, Kd (2.5 mg/kg single dose ip), ABS (1.5 ml/ kg single dose ip), and Kd+ABS (Kd, 2,5 mg/kg single dose ip-ABS, 1.5 ml/kg single dose ip). Lung tissues were evaluated histopathologically. Inflammation was evaluated immunohistochemically with tumor necrosis factor-α (TNF-α). Oxidative stress was evaluated with the total oxidant level (TOS) and total antioxidant level (TAS) using the spectrophotometric method. Apoptosis was evaluated using RT-PCR with relative mRNA fold changes of Bcl-2-associated X (Bax), B-cell lymphoma 2 (Bcl-2), cytochrome c (Cyt c), and caspase 3 genes. Results Histopathological findings such as congestion, hemorrhage, and mononuclear cell infiltration were found to increase in the Cd group. It was found that Cd increased inflammation by increasing TNF-α, increasing TOS and OSI, and decreasing TAS, causing an increase in oxidative stress. (p<0.05). It was determined that there was a significant improvement in all these parameters after the ABS application (p<0.05). Conclusion In conclusion, we suggested that ABS may be an alternative option to protect against Cd-induced lung toxicity, and more research should be done on this subject.

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SDÜ Tıp Fakültesi Dergisi-Cover
  • ISSN: 1300-7416
  • Yayın Aralığı: Yılda 4 Sayı
  • Başlangıç: 2015
  • Yayıncı: Süleyman Demirel Üniversitesi
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