دوره 32، شماره 153 - ( 5-1403 )                   جلد 32 شماره 153 صفحات 298-288 | برگشت به فهرست نسخه ها

Ethics code: IR.KUMS.REC.1400.094


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Abdolmaleki A, Pazhouhi M, Rashidi I, Heshmati S, Jalili C, Khani-Hematabadi F. Molecular Basis of Apoptosis Induced by Taraxasterol on Human Melanoma Cell Line Growth Inhibition: An in-Vitro Study. J Adv Med Biomed Res 2024; 32 (153) :288-298
URL: http://journal.zums.ac.ir/article-1-7415-fa.html
Molecular Basis of Apoptosis Induced by Taraxasterol on Human Melanoma Cell Line Growth Inhibition: An in-Vitro Study. Journal of Advances in Medical and Biomedical Research. 1403; 32 (153) :288-298

URL: http://journal.zums.ac.ir/article-1-7415-fa.html


چکیده:   (721 مشاهده)
Background & Objective: Melanoma, one of the most lethal cancers, originates from epidermal layer. An advanced type of malignant melanoma represents a poor response to chemotherapy or other medications due to intrinsic and/or acquired resistance to antineoplastic drugs. Taraxasterol is a pentacyclic-triterpene agent mainly extracted from Dandelion herb with anti-proliferative and apoptotic features on cancer cells. Thus, this paper investigated the apoptosis pathway caused by Taraxasterol in the human melanoma cell line (hMCL).
Materials & Methods: hMCLs were treated with Taraxasterol and IC50 index was calculated using MTT assay. Then, apoptosis rate was evaluated by DNA Fragmentation Calorimetric technique. Finally, apoptosis pathway was investigated through various molecular laboratory assays.
Results: Low cellular viability level was found as concentration and time-dependent routes. Induction of apoptosis by IC50 value of Taraxasterol was found significantly (p<0.05) effective. Mitochondria membrane potential index was reduced by Taraxasterol significantly (p<0.05). Also, the cytosolic levels of cytochrome C and expression level of caspase 3, 8, and 9 genes in hMCL were increased significantly (p<0.05) following Taraxasterol administration.   
Conclusion: Taraxasterol represents anti-proliferative and toxic effects against hMCL by induction of apoptosis.
 
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نوع مطالعه: مقاله پژوهشی | موضوع مقاله: Life Science
دریافت: 1402/10/10 | پذیرش: 1403/8/14 | انتشار: 1403/5/30

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