Ginsenoside Rh2 Regulates the Calcium/ROS/CK1α/MLKL Pathway to Promote Premature Eryptosis and Hemolysis in Red Blood Cells.

Ginsenoside Rh2 anticancer eryptosis hemolysis oxidative stress

Journal

Toxicologic pathology
ISSN: 1533-1601
Titre abrégé: Toxicol Pathol
Pays: United States
ID NLM: 7905907

Informations de publication

Date de publication:
16 Aug 2024
Historique:
medline: 16 8 2024
pubmed: 16 8 2024
entrez: 16 8 2024
Statut: aheadofprint

Résumé

Ginsenoside Rh2 (GRh2) exhibits significant potential as an anticancer agent; however, progress in developing chemotherapeutic drugs is impeded by their toxicity toward off-target tissues. Specifically, anemia caused by chemotherapy is a debilitating side effect and can be caused by red blood cell (RBC) hemolysis and eryptosis. Cells were exposed to GRh2 in the antitumor range and hemolytic and eryptotic markers were examined under different experimental conditions using photometric and cytofluorimetric methods. GRh2 caused Ca

Identifiants

pubmed: 39148410
doi: 10.1177/01926233241268846
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1926233241268846

Déclaration de conflit d'intérêts

Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Auteurs

Sumiah A Alghareeb (SA)

Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Saud University, Riyadh, Saudi Arabia.

Jawaher Alsughayyir (J)

Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Saud University, Riyadh, Saudi Arabia.

Mohammad A Alfhili (MA)

Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Saud University, Riyadh, Saudi Arabia.

Classifications MeSH