(+)-Columbianetin acetate

(+)-Columbianetin ((S)-Columbianetin) acetate acts as an inhibitor of JNK/ERK. (+)-Columbianetin acetate inhibits UVA-induced phosphorylation of JNK and ERK, reduces the production of MMP-1, reverses UVA-induced Collagen (HY-NP003) degradation, and alleviates UVA-mediated inhibition of Smad2/3 phosphorylation and translocation. (+)-Columbianetin acetate regulates the AP-1 and ASK1-MAPK signaling pathways, inhibits the production of ROS and blocks sub-G₁ cell cycle arrest. (+)-Columbianetin acetate is applicable to research related to skin aging^[1][2]. In Vitro:(+)-Columbianetin acetate (1-25 μM; 48 h) exhibits dose-dependent cytotoxicity in human dermal fibroblasts with an IC₅₀ of 93.89 μM, and maintains >90% cell viability at concentrations up to 10 μM after 48 h incubation^[1].
(+)-Columbianetin acetate (1-10 μM) dose-dependently suppresses UVA (10 J/cm²)-induced reactive nitrogen species generation in human dermal fibroblasts^[1].
(+)-Columbianetin acetate (1-10 μM; 24 h) dose-dependently reverses UVA (10 J/cm²)-induced changes in human dermal fibroblasts, reducing MMP-1 release to 19,094 pg/mL and increasing type Iα1 pro-collagen release to 1,955 pg/mL at 10 μM after 24 h incubation^[1].
(+)-Columbianetin acetate (1-10 μM; 24 h) dose-dependently reverses UVA (10 J/cm²)-induced changes in human dermal fibroblasts, suppressing MMP-1 gene expression and increasing type I pro-collagen gene expression after 24 h incubation^[1].
(+)-Columbianetin acetate (1-10 μM; 48 h) dose-dependently reverses UVA (10 J/cm²)-induced changes in human dermal fibroblasts, suppressing MMP-1 protein expression and increasing type I pro-collagen and collagen protein expression after 48 h incubation^[1].
(+)-Columbianetin acetate (10 μM; 24 h) suppresses UVA (10 J/cm²)-induced phosphorylation of JNK and ERK, but not p38, in human dermal fibroblasts after 24 h incubation^[1].
(+)-Columbianetin acetate (10 μM; 24 h) reverses UVA (10 J/cm²)-induced changes in the TGFβ pathway in human dermal fibroblasts, increasing p-Smad2/3 and Smad4 protein levels and decreasing Smad7 protein levels after 24 h incubation^[1].
(+)-Columbianetin acetate (10 μM; 24 h) increases nuclear levels of p-Smad2/3 and Smad4, reversing UVA (10 J/cm²)-induced reductions in human dermal fibroblasts after 24 h incubation^[1].
(+)-Columbianetin acetate (1-20 μM; 24 h) dose-dependently increases the viability of UVB-exposed HaCaT cells, with near-full viability restoration at 20 μM after 24 h of treatment^[2].
(+)-Columbianetin acetate (1-20 μM; 24 h) dose-dependently reduces UVB-induced cell injury in HaCaT cells, with LDH release suppressed to ~20% of positive control levels at 20 μM after 24 h of treatment^[2].
(+)-Columbianetin acetate (1-20 μM; 2 h) dose-dependently scavenges H₂O₂-induced intracellular ROS in HaCaT cells, with ROS generation reduced to ~72% of H₂O₂-only levels at 20 μM after 2 h of treatment^[2].
(+)-Columbianetin acetate (1-20 μM; 24 h) dose-dependently scavenges UVB-induced intracellular ROS in HaCaT cells, with ROS generation reduced to ~72% of UVB-only levels at 20 μM after 24 h of treatment^[2].
(+)-Columbianetin acetate (1-20 μM; 24 h) dose-dependently reduces UVB-induced sub-G1 phase cell cycle arrest in HaCaT cells, with sub-G1 phase cell percentage lowered to 10.62% at 20 μM after 24 h of treatment^[2].
(+)-Columbianetin acetate (1-20 μM; 24 h) dose-dependently regulates UVB-altered gene expression of MMP-2, MMP-9, TIMP-1, and TIMP-2 in HaCaT cells after 24 h of treatment^[2].
(+)-Columbianetin acetate (1-20 μM; 24 h) dose-dependently regulates UVB-altered protein expression of MMP-2, MMP-9, TIMP-1, and TIMP-2 in HaCaT cells after 24 h of treatment^[2].
(+)-Columbianetin acetate (1-20 μM; 24 h) dose-dependently inhibits UVB-induced phosphorylation of p38, JNK, and ERK MAPKs in HaCaT cells, with the greatest inhibition observed at 20 μM after 24 h of treatment^[2].
(+)-Columbianetin acetate (1-20 μM; 24 h) dose-dependently inhibits UVB-induced phosphorylation of ASK1 in HaCaT cells, with p-ASK1 levels reduced to ~80% of UVB-only levels at 20 μM after 24 h of treatment^[2].
(+)-Columbianetin acetate (1-20 μM; 24 h) dose-dependently inhibits UVB-induced activation of the AP-1 component c-fos in HaCaT cells, with c-fos levels reduced to ~80% of UVB-only levels at 20 μM after 24 h of treatment^[2].
(+)-Columbianetin acetate (1-20 μM; 24 h) dose-dependently inhibits UVB-induced phosphorylation of p53 and upregulation of Bax in HaCaT cells, with the greatest inhibition observed at 20 μM after 24 h of treatment^[2].