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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