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dc.contributor.authorDarendelioglu, E.
dc.date.accessioned2021-04-08T12:06:28Z
dc.date.available2021-04-08T12:06:28Z
dc.date.issued2020
dc.identifier10.4149/BLL_2020_132
dc.identifier.issn00069248
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85095977676&doi=10.4149%2fBLL_2020_132&partnerID=40&md5=da1e0b0a98f073b5e226fd7fddf791bf
dc.identifier.urihttp://acikerisim.bingol.edu.tr/handle/20.500.12898/3951
dc.description.abstractAIM: The purpose of this research was to examine the suppressing effect of caffeic acid (CA) on colon cancer cells triggered by an overdose of H202 and molecular mechanisms involved. METHOD: This study examines cell proliferation, measurement of ROS and lipid peroxidation (LPO) levels, total antioxidant status (TAS) level, catalase (CAT) activity, TUNEL assay for calculating the apoptotic index, immunohistochemical staining for caspase-3 proteins, and qRT-PCR for measuring mRNA levels of apoptotic and anti-apoptotic genes. RESULTS: In this study, CA considerably suppressed HT-29 cell death induced by cytotoxicity achieved by and overdose of H202. Additionally, inducing cells with H202 caused a rise in ROS and LPO levels, decrease in TAS level and CAT activity whereas pre-treatment of cells with CA reversed these effects. Additionally, a considerable increase was observed in the expression of Bax, cas-3, cas-8, cyt c, p53 at mRNA levels after H202 treatment, however, pre-treatment with CA considerably decreased H202-induced upregulation of these genes. CONCLUSION: In light of all these findings, the antioxidant use should be paid attention to as it could decrease the level of ROS, and in turn decrease the apoptotic cell death which is an unwanted situation in the setting of cancer remedy. Overall, these data revealed that CA can suppress apoptosis in HT-29 cells triggered by an overdose of H2O2(Fig. 5, Ref. 37). Text in PDF www.elis.sk © 2020
dc.language.isoEnglish
dc.sourceBratislava Medical Journal
dc.titleCaffeic acid suppresses HT-29 cell death induced by H2O2 via oxidative stress and apoptosis


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