Isolation and identification of α-glucosidase and protein glycation inhibitors from Stereospermum colais.

Stereospermum colais (family Bignoniaceae) is a well-known pharmacologically potent medicinal plant reported in traditional systems of medicine. Phytochemical investigation of the roots of S. colais resulted in the isolation of seven compounds, and the metabolites were screened for its α-glucosidase enzyme inhibition and anti-glycation property. The compounds identified were ß-sitosterol (1), 2-(4'-hydroxyphenyl) ethyl undecanoate (2), 2-(4'-hydroxyphenyl)ethyl pentadecanoate (3), 5α-ergosta-7,22-dien-3ß-ol (4), ursolic acid (5), lapachol (6), and pinoresinol (7). Ursolic acid, lapachol, and pinoresinol possessed IC50 values of 119.01, 130.29, and 125.62 nM, respectively, compared to standard ascorbic acid with an IC50 value of 201.01 nM. The other compounds failed to show the activity. Results of the current study showcased the possible exploration of this medicinal plant for the treatment of type 2 diabetes in line with the development of phytopharmaceutical industry.

In vitro studies to assess the antidiabetic, antiperoxidative, and radical scavenging potential of Stereospermum colais.

CONTEXT: Stereospermum colais (Buch.-Ham. ex Dillw.) Mabberley (Bignoniaceae), which has traditional medicinal properties, is distributed all over deciduous forests. In spite of its many uses, the antidiabetic, antiperoxidative and radical scavenging activities of this species have not been assessed, and its chemical composition is scarcely known. OBJECTIVE: Antidiabetic, antiperoxidation, xanthine oxidase (XO) inhibition, and radical scavenging activities of acetone and methanol extracts of Stereospermum colais roots were investigated. Protective effects of Stereospermum colais root extract in stabilizing sunflower oil was also examined. MATERIALS AND METHODS: The protective effect of acetone (ASC) and methanol (MSC) extracts of Stereospermum colais root for the potential inhibition of α-glucosidase and α-amylase enzymes were studied by in vitro method. Glycation inhibitory activity was also studied to inhibit the production of glycated end products. RESULTS: Compared with acarbose, ASC showed a strong inhibitory activity against α-glucosidase (IC(50) 61.21 µg/mL) and a moderate inhibitory activity against α-amylase (IC(50) 681.08 µg/mL). Glycation inhibitory activity of Stereospermum colais root extracts by using an in vitro glucose-bovine serum albumin (BSA) assay was also done and compared with standard gallic acid. ASC also shows high XO inhibition potential, free radical scavenging activities, and low p-anisidine value indicates the high medicinal potency of Stereospermum colais root. DISCUSSION AND CONCLUSION: These results suggest that the extract of Stereospermum colais may be interesting for incorporation in pharmaceutical preparations for human health, since it can suppress hyperglycaemia, and or as food additives due to its antiradical efficiency.

Inhibitory potential of ginger extracts against enzymes linked to type 2 diabetes, inflammation and induced oxidative stress.

Ginger (Zingiber officinale Roscoe) continues to be used as an important cooking spice and herbal medicine around the world. Gingerols, the major pungent components of ginger, are known to improve diabetes, including the effect of enhancement against insulin sensitivity. In the current study, ginger sequentially extracted with different solvents-namely, hexane, ethyl acetate, methanol, 70% methanol-water and water-were screened to determine the variations in phenolic-linked active constituents. The potential of these extracts to inhibit key enzymes relevant to type 2 diabetes and inflammation was studied. Phenolic compounds-namely, gingerols and shoagols-were quantified using high-performance liquid chromatography. Ethyl acetate extract showed higher activity compared with other extracts. These studies indicate that ginger has very good potential for α-glucosidase and α-amylase inhibition relevant for type 2 diabetes management and cyclooxygenase inhibition for inflammation.