SKF-38393
SKF-38393 has been studied in 1 paper since 2023: none in people yet, 1 in cells. No study of it in people or animals has been published yet. The newest paper, Mar 7, 2023: “Dopamine D1 receptor activation ameliorates ox-LDL-induced endothelial cell senescence via CREB/Nrf2 pathway”.
- 1 lab in 1 country
- Funder: Natural Science Foundation of Heilongjiang Province
- Cells1
What did studies of SKF-38393 find?
3Studies of SKF-38393 measured 3 outcomes; the most studied are NRF2–KEAP1 antioxidant response (1 study), cellular senescence (1) and oxidative stress and ROS signaling (1).
NRF2–KEAP1 antioxidant response
upin human cells1
1 study
NRF2–KEAP1 antioxidant response
upin human cells1
SKF-38393 activates NRF2–KEAP1 antioxidant response in human cells.
“SKF38393 increased the phosphorylation of cAMP response element-binding protein (CREB) at serine-133, nuclear accumulation of nuclear factor erythroid 2-related factor 2 (Nrf2) and expression of HO-1 in HUVECs.”
Cellsin HUVECs
Experimental cell research
Cellular senescence
downin human cells1
1 study
Cellular senescence
downin human cells1
SKF-38393 decreases cellular senescence in human cells.
“Increased proportion of senescence-associated β-galactosidase (SA-β-gal) positive staining cells and activated p16/p21/p53 pathway in ox-LDL-treated HUVECs were significantly abolished by DR1 activation.”
Cellsin ox-LDL-treated HUVECs
Experimental cell research
Oxidative stress and ROS signaling
downin human cells1
1 study
Oxidative stress and ROS signaling
downin human cells1
SKF-38393 decreases oxidative stress and ROS signaling in human cells.
“elevated Prx hyperoxidation and reactive oxygen species (ROS) levels in ox-LDL-treated Human umbilical vein endothelial cells (HUVECs) were observed, suppressed by DR1 agonist SKF38393.”
Cellsin ox-LDL-treated HUVECs
Experimental cell research