Fenofibric acid serves as an activator for PPAR, exhibiting EC50s of 22.4 µM, 1.47 µM, and 1.06 µM for PPARα, PPARγ, and PPARδ, respectively[1]. At concentrations ranging from 10 to 100 nM, Fenofibric acid progressively inhibits the COX-2 enzyme, achieving an IC50 of 48 nM[2]. At a concentration of 500 nM, Fenofibric acid leads to a reduction in the levels of AOX1 protein in HepG2 cells[3]. Fenofibric acid at 100 µM reduces phosphorylation of JNK1/2, c-Jun, and p38 MAPK, and protects against the build-up of reactive oxygen species, endoplasmic reticulum (ER) stress, and damage to the blood retinal barrier (BRB) triggered by a combination of high-glucose and hypoxic conditions in ARPE-19 cells. Additionally, at this concentration, Fenofibric acid stimulates the IGF-IR/Akt/ERK1/2-mediated survival signaling pathways in ARPE-19 cells under these stress conditions[4].
体内研究
Fenofibric acid, administered orally in doses of 1, 5, and 10 mg/kg, demonstrates anti-inflammatory effects in Wistar rats suffering from acute inflammation induced by carrageenan[2].
体外研究
Fenofibric acid serves as an activator for PPAR, exhibiting EC50s of 22.4 µM, 1.47 µM, and 1.06 µM for PPARα, PPARγ, and PPARδ, respectively[1].
At concentrations ranging from 10 to 100 nM, Fenofibric acid progressively inhibits the COX-2 enzyme, achieving an IC50 of 48 nM[2].
At a concentration of 500 nM, Fenofibric acid leads to a reduction in the levels of AOX1 protein in HepG2 cells[3].
Fenofibric acid at 100 µM reduces phosphorylation of JNK1/2, c-Jun, and p38 MAPK, and protects against the build-up of reactive oxygen species, endoplasmic reticulum (ER) stress, and damage to the blood retinal barrier (BRB) triggered by a combination of high-glucose and hypoxic conditions in ARPE-19 cells. Additionally, at this concentration, Fenofibric acid stimulates the IGF-IR/Akt/ERK1/2-mediated survival signaling pathways in ARPE-19 cells under these stress conditions[4].
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