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Molecular Mechanism of Apoptotic Cell Death in Cyanidin-3-glucoside-induced Cytotoxic Potential on Human Liver Carcinoma (HepG2) Cell Line (Record no. 130089)

MARC details
000 -LEADER
fixed length control field 02426nam a2200169 4500
008 - FIXED-LENGTH DATA ELEMENTS--GENERAL INFORMATION
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100 ## - MAIN ENTRY--PERSONAL NAME
Personal name Suresh Mickymaray
245 ## - TITLE STATEMENT
Title Molecular Mechanism of Apoptotic Cell Death in Cyanidin-3-glucoside-induced Cytotoxic Potential on Human Liver Carcinoma (HepG2) Cell Line
300 ## - PHYSICAL DESCRIPTION
Extent P 254-262
520 ## - SUMMARY, ETC.
Summary, etc. biblio.abstract Background: Liver cancer is one of the most prevalent cancers around the world and the leading cause of cancer-related deaths. Because liver cancer prevalence has increased significantly, there are no established therapies, and there are serious adverse reactions associated with the use of medications already available, new and more potent anticancer agents must be investigated. Aim: Using in vitro methods, we have assessed Cyanidin-3-glucoside (C3gc)'s anticancer activities and the underlying molecular mechanisms. Materials and Methods: In the current investigation, the cytotoxicity and apoptotic activity of C3gc against liver cancer cell line HepG2, has been investigated using MTT assay, LDH release assay, AO/EtBr dual staining, DAPI staining, ROS estimation, Mitochondrial ATPase assay, and oxidative stress parameters has been examined. Results: Assays of MTT and LDH release showed that C3gc exhibited cytotoxic potential and cell membrane distribution by reducing cell viability dose-dependently. The AO/EB and DAPI staining techniques were used to assess morphological changes associated with apoptosis, confirming its apoptotic nature. In HepG2 cell lines, C3gc increased ROS generation and ATPase activity. Furthermore, C3gc-treated cells showed a significant increase in MDA levels while decreasing SOD and GSH levels. This reflects increased oxidative stress and decreased antioxidant activity in HepG2 cells. Conclusion: C3gc inhibits cancer cell proliferation by enhancing ROS levels, disrupting cell membrane integrity, and causing DNA fragmentation and apoptosis through oxidative stress-mediated pathways. Thus, C3gc could be effectively utilized as an effective anti-cancer alternative for liver cancer.
654 ## - SUBJECT ADDED ENTRY--FACETED TOPICAL TERMS
Subject <a href=" Liver cancer"> Liver cancer</a>
-- <a href="Cyanidin-3-glucoside">Cyanidin-3-glucoside</a>
-- <a href=" HepG2 cells"> HepG2 cells</a>
-- <a href="Reactive oxygen species">Reactive oxygen species</a>
-- <a href="Apoptosis">Apoptosis</a>
773 0# - HOST ITEM ENTRY
Host Biblionumber 125266
Host Itemnumber 109601
Place, publisher, and date of publication Banglore Association of Pharmaceutical Tearchers of India
Title Indian Journal of Pharmaceutical Education and Research
International Standard Serial Number 0019-5464
942 ## - ADDED ENTRY ELEMENTS (KOHA)
Koha item type Journal Article
773 0# - HOST ITEM ENTRY
-- JP44
942 ## - ADDED ENTRY ELEMENTS (KOHA)
-- ddc
Holdings
Withdrawn status Lost status Source of classification or shelving scheme Damaged status Not for loan Location (home branch) Sublocation or collection (holding branch) Date acquired Koha issues (times borrowed) Piece designation (barcode) Koha date last seen Price effective from Koha item type
    Dewey Decimal Classification     SNDT Juhu SNDT Juhu 11/11/2024   JP44.28 11/11/2024 11/11/2024 Journal Article