Santamarine

Santamarine (Santamarin; Balchanin) is a sesquiterpene lactone found in Artemisia scoparia. Santamarine shows anti-inflammatory, antioxidant, anticancer and anti-photoaging activities. Santamarine suppresses UVA-induced phosphorylation of JNK and p38 MAPK, nuclear translocation of phosphorylated c-Fos and c-Jun, and AP-1-mediated MMP-1 transcription and secretion. Santamarine suppresses NF-κB signaling, iNOS, COX-2, TNF-α, and IL-1β production. Santamarine inhibits thioredoxin reductase activity, induces ROS production, mitochondrial apoptosis, G2/M cell cycle arrest, and DNA damage, and reduces cancer cell growth. Santamarine can be used for the photoaging, inflammatory diseases and cancer^[1][2][3][4]. In Vitro:Santamarine (1-10 μM; 1 h) scavenges intracellular ROS in HDFs with an IC₅₀ of 4.04 μM^[1].
Santamarine (1-10 μM; 24 h) dose-dependently reduces UVA-induced MMP-1 secretion in HDFs, with a significant reduction to 33.00 ng/mL at 10 μM^[1].
Santamarine (1-10 μM; 24 h) dose-dependently downregulates UVA-induced MMP-1, -3, -9 mRNA and protein expression in HDFs^[1].
Santamarine (1-10 μM; 24 h) dose-dependently stimulates type I procollagen mRNA and protein expression in UVA-irradiated HDFs^[1].
Santamarine (10 μM; 24 h) suppresses UVA-induced activation of the p38/JNK MAPK pathway and nuclear translocation of AP-1 complex components p-c-Fos and p-c-Jun in HDFs^[1].
Santamarine (10 μM; 24 h) activates the TGF-β/Smad pathway in UVA-irradiated HDFs by restoring TGF-β levels, increasing Smad2/3 phosphorylation, reducing Smad7 levels, and elevating nuclear p-Smad2/3 and Smad4 levels^[1].
Santamarine (1-10 μM; 24 h) dose-dependently stimulates Nrf2-dependent expression of antioxidant enzymes SOD-1 and HO-1 in UVA-irradiated HDF^[1].
Santamarin (5-80 μM; 24 h) does not significantly reduce RAW264.7 cell viability at concentrations up to 40 μM^[2].
Santamarin (5-40 μM; 12 h) concentration-dependently reduces iNOS and COX-2 protein expression in LPS (HY-D1056)-stimulated RAW264.7 cells^[2].
Santamarin (5-40 μM; 12 h) concentration-dependently reduces nitrite, PGE₂, TNF-α, and IL-1β production in LPS-stimulated RAW264.7 cells^[2].
Santamarin (5-40 μM; 12 h) concentration-dependently inhibits LPS-induced IκB-α phosphorylation/degradation, p65 nuclear translocation, and NF-κB DNA binding activity in RAW264.7 cells^[2].
Santamarin (5-40 μM; 12 h) concentration-dependently increases HO-1 mRNA and protein expression, and HO enzyme activity in RAW264.7 cells^[2].
Santamarin (40 μM; 0.5-1.5 h) induces a time-dependent nuclear translocation of Nrf2 in RAW264.7 cells over 0.5 to 1.5 h of incubation^[2].
Santamarine (10-100 μM; 24 h) dose-dependently inhibits the growth of A549 and NCI-H1650 lung adenocarcinoma cells (IC₅₀ = 45 μM and 43 μM, respectively) and is far less toxic to NL-20 normal lung cells (IC₅₀ = 85 μM)^[3].
Santamarine (40-60 μM; 24 h) induces dose-dependent cell death, apoptosis and associated morphological changes in A549 and NCI-H1650 lung adenocarcinoma cells and these changes are reversed by the ROS scavenger NAC (HY-B0215)^[3].
Santamarine (40-60 μM; 1-24 h) induces ROS generation (maximal at 4 h) in A549 lung adenocarcinoma cells, with no detectable change in ROS levels after 24 h treatment^[3].
Santamarine (40-60 μM; 24 h) dose-dependently reduces the intracellular GSH/GSSG ratio in A549 lung adenocarcinoma cells and this effect is reversed by the ROS scavenger NAC^[3].
Santamarine (40-60 μM; 24 h) dose-dependently inhibits thioredoxin reductase activity in A549 lung adenocarcinoma cells and this effect is reversed by the ROS scavenger NAC^[3].
Santamarine (40-60 μM; 24 h) dose-dependently induces oxidative stress-mediated mitochondrial apoptosis in A549 lung adenocarcinoma cells via modulation of Bcl-2 family proteins, dissipation of mitochondrial membrane potential, and activation of caspase-3 and PARP cleavage, with all effects reversed by the ROS scavenger NAC^[3].
Santamarine (40-60 μM; 24 h) dose-dependently inhibits constitutive and TNF-α-induced NF-κBp65 nuclear translocation and IκB-α phosphorylation in A549 lung adenocarcinoma cells via an oxidative stress-dependent mechanism^[3].
Santamarine (0-25 μg/mL; 24 h) selectively inhibits viability of OC-2 and HSC-3 oral cancer cells, with IC₅₀ values of 15.7 μg/mL and 18.49 μg/mL after 24 h treatment, while having minimal effect on normal S-G cells, and this selective activity is oxidative stress-dependent^[4].
Santamarine (15-25 μg/mL; 24 h) induces G2/M cell cycle arrest in OC-2 and HSC-3 oral cancer cells after 24 h treatment at 15 and 25 μg/mL, while causing only minor changes in normal S-G cells^[4].
Santamarine (15-25 μg/mL; 12-24 h) dose-dependently and time-dependently induces apoptosis and activates caspase 3, 8, 9 in OC-2 and HSC-3 oral cancer cells, while having minimal effect on normal S-G cells^[4].
Santamarine (15-25 μg/mL; 12-24 h) dose-dependently and time-dependently induces ROS, mitochondrial superoxide generation and MMP, GSH depletion in OC-2 and HSC-3 oral cancer cells, while having minimal effect on normal S-G cells^[4].
Santamarine (15-25 μg/mL; 12-24 h) dose-dependently and time-dependently induces γH2AX- and 8-OHdG-mediated DNA damage in OC-2 and HSC-3 oral cancer cells, while having minimal effect on normal S-G cells^[4].