Homoplantaginin |cas 17680-84-1

Homoplantaginin |cas 17680-84-1

DC Chemicals, Website: www.dcchemicals.com

Product Name: Homoplantaginin|Cas Number: 17680-84-1| Catalog Number: DC10177

Homoplantaginin is a flavonoid from a traditional Chinese medicine Salvia plebeia with antiinfammatory and antioxidant properties.

Homoplantaginin shows IC50 of reduction level of DPPH radical at 0.35 μg/mL. In human hepatocyte HL-7702 cells exposed to H2O2, the addition of 0.1-100μg/mL of homoplantaginin significantly reduces lactate dehydrogenase leakage, and increases glutathione, glutathione peroxidase and superoxide dismutase in supernatant[1]. Homoplantaginin (0.1, 1, 10 μM) dose-dependently reduces expression of toll-like receptor-4 evoked by palmitic acid (100 μM). Homoplantaginin tightly controlls palmitic acid-induced reactive oxygen species to prevent nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome activation by suppressing reactive oxygen species-sensitive thioredoxin-interacting protein, NLRP3, and caspase-1[2]. Pre-treatment of homoplantaginin on human umbilical vein endothelial cells significantly inhibits palmitic acid induced TNF-α and IL-6 mRNA expression, and IKKβ and NF-κB p65 phosphorylation. Homoplantaginin significantly modulates the Ser/Thr phosphorylation of IRS-1, improves phosphorylation of Akt and endothelial nitric oxide synthase, and increases NO production in the presence of insulin[3].Homoplantaginin shows IC50 of reduction level of DPPH radical at 0.35 μg/mL. In human hepatocyte HL-7702 cells exposed to H2O2, the addition of 0.1-100μg/mL of homoplantaginin significantly reduces lactate dehydrogenase leakage, and increases glutathione, glutathione peroxidase and superoxide dismutase in supernatant[1]. Homoplantaginin (0.1, 1, 10 μM) dose-dependently reduces expression of toll-like receptor-4 evoked by palmitic acid (100 μM). Homoplantaginin tightly controlls palmitic acid-induced reactive oxygen species to prevent nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome activation by suppressing reactive oxygen species-sensitive thioredoxin-interacting protein, NLRP3, and caspase-1[2]. Pre-treatment of homoplantaginin on human umbilical vein endothelial cells significantly inhibits palmitic acid induced TNF-α and IL-6 mRNA expression, and IKKβ and NF-κB p65 phosphorylation. Homoplantaginin significantly modulates the Ser/Thr phosphorylation of IRS-1, improves phosphorylation of Akt and endothelial nitric oxide synthase, and increases NO production in the presence of insulin[3].