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

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dc.contributor.authorTepebaşı, Muhammet Yusuf
dc.contributor.authorSezgıner, Perıhan
dc.date.accessioned2026-01-24T12:01:28Z
dc.date.available2026-01-24T12:01:28Z
dc.date.issued2023
dc.departmentAlanya Alaaddin Keykubat Üniversitesi
dc.description.abstractObjective 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, anti- inflammatory, 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-? (TNF-?). 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-?, 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.
dc.identifier.doi10.17343/sdutfd.1278783
dc.identifier.endpage233
dc.identifier.issn1300-7416
dc.identifier.issn2602-2109
dc.identifier.issue2
dc.identifier.startpage225
dc.identifier.trdizinid1182570
dc.identifier.urihttps://search.trdizin.gov.tr/tr/yayin/detay/1182570
dc.identifier.urihttps://doi.org/10.17343/sdutfd.1278783
dc.identifier.urihttps://hdl.handle.net/20.500.12868/4329
dc.identifier.volume30
dc.indekslendigikaynakTR-Dizin
dc.language.isoen
dc.relation.ispartofSüleyman Demirel Üniversitesi Tıp Fakültesi Dergisi
dc.relation.publicationcategoryMakale - Ulusal Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_TR-Dizin_20260121
dc.subjectLung
dc.subjectOxidative stress
dc.subjectApoptosis
dc.subjectCadmium
dc.subjectAnkaferd Blood Stopper
dc.subjectİnflammation
dc.titleANKAFERD BLOOD STOPPER ALLEVIATES CADMIUM-INDUCED LUNG INJURY BY REDUCING MITOCHONDRIAL STRESS-RELATED APOPTOSIS VIA BAX/BCL-2 AND CYT-C/CAS-3 PATHWAYS
dc.typeArticle

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