Sargachromanol E

Sargachromanol E is an apoptosis inducer, growth inhibitor, anti-inflammatory agent, and anti-aging agent. Sargachromanol E activates caspase-3, mediates PARP cleavage, downregulates Bcl-xL and upregulates Bax levels, and promotes cell cycle arrest at the sub-G1 phase. It inhibits LPS-induced transcription and expression of COX-2 and iNOS (NO: IC₅₀ = 6.99 μg/mL), reduces the phosphorylation levels of p38 MAPK and ERK1/2, and suppresses the release of pro-inflammatory mediators including TNF‑α, IL‑1β, and prostaglandin E₂. Sargachromanol E can be used in research related to leukemia, oral squamous cell carcinoma, and inflammation^[1][2][3][4]. In Vitro:Sargachromanol E (SE) (12.5-50 μM; 24 h) potently inhibits the proliferation of human promyelocytic leukemia HL-60 cells in vitro in a dose-dependent manner, with inhibition rates of 10.7%, 68.9% and 90.1% at concentrations of 12.5, 25 and 50 μM, respectively, and exhibits no cytotoxicity against normal cell lines at these concentrations^[1].
Sargachromanol E (12.5-50 μM; 24 h) induces nuclear pyknosis and fragmentation in human promyelocytic leukemia HL-60 cells^[1].
Sargachromanol E (12.5-50 μM; 24 h) induces apoptotic DNA fragmentation in human promyelocytic leukemia HL-60 cells^[1].
Sargachromanol E (12.5-25 μM; 24 h) regulates the expression of apoptosis-related proteins in human promyelocytic leukemia HL-60 cells; at concentrations of 12.5 μM and 25 μM, slight upregulation of Bax, significant downregulation of Bcl-xL, activation of caspase-3 and caspase-9, and cleavage of PARP are observed^[1].
Apoptosis induced by Sargachromanol E (25 μM; 24 h) in human promyelocytic leukemia HL-60 cells is attenuated by the caspase-3 inhibitor Z-DEVD-fmk (HY-12466)^[1].
Sargachromanol E (12.5-50 μM; 24 h) induces a concentration-dependent increase in apoptotic sub-G₁ hypodiploid cells without affecting the progression of the G₂/M phase in human promyelocytic leukemia HL-60 cells^[1].
Sargachromanol E (5-25 μg/mL; pre-treatment for 2 h) potently inhibits NO production in LPS-stimulated RAW 264.7 macrophages, with an IC₅₀ of 6.99 μg/mL, and shows no cytotoxicity even at concentrations as high as 25 μg/mL^[2].
Sargachromanol E (16.3 μM) inhibits NO production in LPS-stimulated mouse RAW 264.7 macrophages, with an IC₅₀ value of 16.3 μM^[4].
Sargachromanol E (5-25 μg/mL; pre-treatment for 2 h) dose-dependently inhibits the production of PGE₂, TNF-α, and IL-1β, reduces the protein expression of COX-2 and iNOS, suppresses the phosphorylation of ERK1/2 and JNK, and mildly decreases the phosphorylation of p38 in LPS-stimulated RAW 264.7 macrophages^[2].
Sargachromanol E induces caspase-3-mediated apoptosis in promyelocytic leukemia HL-60 cells^[4].
Sargachromanol E inhibits long-wave ultraviolet-induced senescence in human skin fibroblasts^[4].