The amino acid and fatty acid composition of polypeptide k and oil isolated from the seeds of Momordica charantia was analysed. The analysis revealed polypeptide k contained 9 out of 11 essential amino acids, among a total of 18 types of amino acids. Glutamic acid, aspartic acid, arginine and glycine were the most abundant (17.08%, 9.71%, 9.50% and 8.90% of total amino acids, respectively). Fatty acid analysis showed unusually high amounts of C18-0 (stearic acid, 62.31% of total fatty acid). C18-1 (oleic acid) and C18-2 (linoleic acid) were the other major fatty acid detected (12.53% and 10.40%, respectively). The oil was devoid of the short fatty acids (C4-0 to C8-0). Polypeptide k and oil were also subjected to in vitro α-glucosidase and α-amylase inhibition assays. Both polypeptide k and seed oil showed potent inhibition of α-glucosidase enzyme (79.18% and 53.55% inhibition, respectively). α-Amylase was inhibited by 35.58% and 38.02%, respectively. Collectively, the in vitro assay strongly suggests that both polypeptide k and seed oil from Momordica charantia are potent potential hypoglycemic agents.

Histamine is established as a potent inflammatory mediator and it is known to increased endothelial permeability by promoting gap formation between endothelial cells. Previous studies have shown that aqueous extract of Bixa orellana leaves (AEBO) exhibits antihistamine activity in vivo, yet the mechanism of its action on endothelial barrier function remains unclear. Therefore, the current study aimed to determine the protective effect of AEBO against histamine-induced hyperpermeability in vitro. The endothelial protective effect of AEBO was assess using an in vitro vascular permeability assay kit. Human umbilical vein endothelial cells (HUVEC) were used in the current study. HUVEC were pre-treated with AEBO for 12 h before histamine induction. Vascular permeability was evaluated by the amount of FITC-dextran leakage into the lower chamber. In order to elucidate the mechanism of action of AEBO, phospholipase C (PLC) activity, intracellular calcium level, nitric oxide (NO) concentration, cyclic guanosine monophosphate (cGMP) production and protein kinase C (PKC) activity were determined following histamine challenge. Histamine-induced increased HUVEC permeability was significantly attenuated by pretreatment with AEBO in a time- and concentration-dependent manner. Upregulation of PLC activity caused by histamine in HUVEC was suppressed by pretreatment with AEBO. Pretreatment with AEBO also blocked the production of intracellular calcium induced by histamine in HUVEC. In addition, AEBO suppressed the NO-cGMP signaling cascade when HUVEC were challenged with histamine. Moreover, PKC activity was significantly abolished by pretreatment with AEBO in HUVEC under histamine condition. In conclusion, the present data suggest that AEBO could suppress histamine-induced increased endothelial permeability and the activity may be closely related with the inhibition of the PLC-NO-cGMP signaling pathway and PKC activity.