1. Naringin inhibits some drug-metabolizing cytochrome P450 enzymes, including CYP3A4 and CYP1A2, which may result in drug-drug interactions.
2. Naringin has protective effects against cognitive dysfunction and reduces diabetes-induced neuropathy in rats.
3. Naringin is an inhibitor of vascular endothelial growth factor (VEGF) release, which causes angiogenesis.
4. Naringin has antioxidant properties in its cardioprotective effects in various models, by providing cardioprotection by inducing the phosphorylation of ERK1/2, PKCδ, and AKT, which subsequently activated Nrf2 and its downstream genes.
1. Ginsenoside Rg2 has a neuroprotective effect against glutamate-induced neurotoxicity through mechanisms related to anti-oxidation and anti-apoptosis.
2. Ginsenoside Rg2 may be as a potential treatment strategy for Alzheimer's disease by inhibiting the formation of Abeta1-40.
3. Ginsenoside Rg2 inhibits nicotinic acetylcholine receptor-mediated Na+ influx and channel activity.
4. Ginsenoside Rg2 may regulate the 5-HT3A receptors that are expressed in Xenopus oocytes.
5. Ginsenoside Rg2 may inhibit or prevent the growth of tumors.
1. Isoferulic acid is an effective natural antioxidant in both lipid and aqueous media.
2. Isoferulic acid efficiently inhibits both monophenolase and diphenolase activities of mushroom tyrosinase .
3. Isoferulic acid has inhibitory effect on fructose- and glucose-mediated protein glycation and oxidation of bovine serum albumin.
4. Isoferulic acid might be a new promising anti-glycation agent for the prevention of diabetic complications via inhibition of AGEs formation and oxidation-dependent protein damage.
1. Ginsenoside Rg2 can protect H9c2 cells against H2O2- induced injury through its actions of anti-oxidant and anti-apoptosis.
2. Ginsenoside Rg2 suppresses the hepatic glucose production via AMPK-induced phosphorylation of GSK3βand induction of SHP gene expression, it may have a therapeutic potential for type 2 diabetic patients.
3. 20R-Ginsenoside Rg2 inhibits the cytokine interleukin 1 alpha (IL-1α)-induced reduction in gap junction-mediated intercellular communication (GJIC).