Ankaferd blood stopper bax/bcl-2 ve cyt-c/cas-3 yolaklari araciliğiyla mitokondriyal stresle ilişkili apoptozu azaltarak kadmiyum kaynakli akciğer hasarini hafifletir

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