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A novel continuous-progression CKM model combined with multi-omics data integration identifies lipid metabolic drivers of disease progression
Abstract Introduction: Cardiovascular–kidney–metabolic (CKM) syndrome represents an emerging systemic disorder characterized by intertwined metabolic dysfunction, chronic kidney disease, and cardiovascular injury, yet robust preclinical models and mechanistic insights remain limited.
The identification of molecular target of (20S) ginsenoside Rh2 for its anti-cancer activity
HepG2, and HEK-293T cells were obtained from the American Type Culture Collection (ATCC, Rockville, MA, USA). Dulbecco’s Modified Eagle Medium (DMEM) was obtained from Gibco BRL (Grand Island, NE, USA). The following reagents were used: (20S)G-Rh2 (Sigma), (20R)G-Rh2 (Sigma), phorbol myristate acetate (PMA. Sigma), and etoposide (Sigma). The ginsenosides were dissolved in 75% alcohol. PMA and etoposide were dissolved in DMSO.
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