5,7-Dihydroxy-4-methylcoumarin

5,7-Dihydroxy-4-methylcoumarin is an antioxidant. 5,7-Dihydroxy-4-methylcoumarin protects mouse cochlear hair cells from Cisplatin-induced damage, enhances cell viability and inhibits apoptosis. 5,7-Dihydroxy-4-methylcoumarin downregulates phosphorylated JNK levels, increases the ratio of phosphorylated FoxO1 to total FoxO1, scavenges free radicals, reduces ROS accumulation, maintains mitochondrial membrane potential and alleviates mitochondrial dysfunction. 5,7-Dihydroxy-4-methylcoumarin downregulates the expression of caspase-3 and improves cell viability. 5,7-Dihydroxy-4-methylcoumarin can be used in studies related to ototoxicity^[1][2]. In Vitro:5,7-Dihydroxy-4-methylcoumarin (D4M) (50-150 μM; 2 h pretreatment followed by 24 h co-treatment with Cisplatin) dose-dependently increases the viability of HEI-OC1 cells exposed to Cisplatin (HY-17394), with the strongest protective effect observed at 100 μM^[1].
5,7-Dihydroxy-4-methylcoumarin (100 μM; 2 h pretreatment followed by 24 h co-treatment with Cisplatin) protects hair cells in the apical, middle and basal turns of cochlear explants from postnatal day 3 C57BL/6 mice against Cisplatin-induced loss, reduces mitochondrial ROS accumulation in cells, and preserves spiral ganglion neurons in the middle turn^[1].
5,7-Dihydroxy-4-methylcoumarin (100 μM; 2 h pretreatment followed by 24 h co-treatment with Cisplatin) inhibits Cisplatin-induced apoptosis of HEI-OC1 cells by downregulating the expression of caspase-3^[1].
5,7-Dihydroxy-4-methylcoumarin (100 μM; 2 h pretreatment followed by 24 h co-treatment with cisplatin) downregulates the phosphorylation level of JNK, reduces the activation and nuclear localization of FoxO1 in HEI-OC1 cells exposed to cisplatin, inhibits mitochondrial ROS accumulation, and maintains mitochondrial membrane potential^[1].