Colorless crystals, soluble in organic solvents such as methanol, ethanol, and DMSO, derived from the dried roots of Panax notoginseng.
Dencichin is a non-protein amino acid originally extracted from Panax notoginseng, and can inhibit HIF-prolyl hydroxylase-2 (PHD-2) activity.
ChEBI: An Nbeta-acyl-L-2,3-diaminopropionic acid in which the acyl group is oxalyl.
β-ODAP is a potent inhibitor of HIF-prolyl hydroxylase-2 (PHD-2) th at induces HIF dependent HRE (hypoxia response element) in normoxic conditions. β-ODAP is an analog of glutamic acid present in Lathyrus sativus (grass pea) th at activates AMPA receptors. β-ODAP causes neurolathyrism upon prolonged consumption of L. sativus seeds.', 'β-ODAP is considered more neurotoxic than α-ODAP, thus during food processing, its conversion to α isomer is essential. β-ODAP exhibits its neurotoxicity via the activation of metabotropic glutamatergic receptor.
Dencichin improves metabolism disorder in diabetic nephropathy (DN) secondary to type II diabetes mellitus (DM) model. Dencichin (80, 160 mg/kg/day, p.o.) significantly prevents the up-regulation of TCH, TG, LDL, and HbAlc and the down-regulation of HDL in DN rats induced by STZ injection. Dencichin also attenuates renal injury induced in the DN secondary to type II DM model. Dencichin alleviates pancreas damage in the STZ-induced DN model. Dencichin regulates protein expression in the TGF-β/Smad signalling pathway in STZ-induced DN models[2].
[1] Eslavath RK, et al. β-N-oxalyl-L-α, β- diaminopropionic acid induces HRE expression by inhibiting HIF-prolyl hydroxylase-2 in normoxic conditions. Eur J Pharmacol. 2016 Nov 15;791:405-411. DOI:
10.1016/j.ejphar.2016.07.007[2] Jie L, et al. Dencichine ameliorates kidney injury in induced type II diabetic nephropathy via the TGF-β/Smad signalling pathway. Eur J Pharmacol. 2017 Oct 5;812:196-205. DOI:
10.1016/j.ejphar.2017.06.024
