Anti-oxidative and anti-hyperglycemic properties of Agastache foeniculum essential oil and oily fraction in hyperglycemia-stimulated and lipopolysaccharide-stimulated macrophage cells: In vitro and in silico studies.

ETHNOPHARMACOLOGICAL RELEVANCE: Hyperglycemia (HG) and lipopolysaccharide (LPS) often promote superoxide accumulation, which may increase oxidative stress. Reducing superoxide production in hyperglycemia and the inflammatory condition is an emerging way to reduce protein and lipid oxidation and diabetes complication. AIM OF STUDY: To examine the effect of Agastache foeniculum essential oil (AFEO) and oil fraction (AFoil) on HG- and LPS-stimulated oxidative stress, the pathogenicity of AFEO and AFoil on oxidative stress was assessed. METHODS: The stimulatory effects of AFEO and AFoil on the activity and expression of NADH oxide (NOX), catalase (CAT), superoxide dismutase (SOD), and the expression of nuclear respiratory factor 2 (NRF2) and nuclear factor-kappa B (NF-kB) in the stimulated macrophage cell line, J774.A1, was studied. The interaction patterns of AFEO and AFoil components with NOX, SOD, CAT, NRF2, and NF-kB proteins were also deduced using molecular docking. RESULTS: Estragole was the main ingredient in AFEO (97%). Linolenic acid (32.10%), estragole (16.22%), palmitic acid (12.62%), linoleic acid (12.04%), and oleic acid (8.73%) were the major chemical components of the AFoil. NOX activation was stimulated in macrophage cells by HG and LPS. At 20 µg/mL, AFEO and AFoil decreased NOX activity while increased SOD and CAT activities in stimulated macrophages. AFoil with estragole and omega-3 fatty acids was better than AFEO with estragole in anti-hyperglycemic and anti-oxidative activity. According to molecular docking research, estragole, linoleic acid, and linolenic acid bind to different hydrophobic pockets of NOX, SOD, CAT, NFR2, and NF-kB using hydrogen bonds, van der Waals bonds, pi-alkyl, and pi-anion interactions, with different binding energies. CONCLUSION: AFEO and AFoil showed antioxidant and anti-diabetic activity. The mechanisms in lowering oxidative stress markers depended on down-regulating superoxide-producing enzymes and up-regulating superoxide-removing enzymes at gene and protein levels. The AFoil emulsion can be used to reduce the detrimental impacts of hyperglycemia and oxidative stress.

In vitro antioxidant and antidiabetic activity of essential oils encapsulated in gelatin-pectin particles against sugar, lipid and protein oxidation and amylase and glucosidase activity.

The in vitro antioxidant and antidiabetic activities of Oliveria decumbens, Thymus kotschyanus, Trachyspermum ammi, and Zataria multiflora essential oils incorporated into gelatin-pectin composite were investigated. The gas chromatography-mass spectrometry characterization revealed that thymol (1.2%-86.4%), carvacrol (3.2%-52.4%), gamma-terpinene (0.0%-12.7%), para-cymene (3.2%-5.2%), geraniol (0.0%-14.5%), and spathulenol (0.0%-13.6%) are the major constituents of the essential oils. Gelatin-pectin composite incorporated with the essential oils exhibited acidic pH (2.40-3.04), low conductivity (265-278 µS/cm), low surface tension (19.0-23.5 mN/m), low Newtonian viscosity (23.7-28.5 mPa.s), negative zeta-potential (14.2-16.9 mV), and nanoscale particle size (313-336 nm). These rheological properties result in the production of globular gelatin-pectin nanoparticles with a size range of 500-700 nm. The FTIR spectra of gelatin-pectin and gelatin-pectin-essential oils to some extent were similar, suggesting the noncovalent interactions between them. Gelatin-pectin composite incorporated with the essential oils displayed antiglucose oxidation (130-150 µg/ml) antilipid peroxidation (120-130 µg/ml), antiprotein oxidation (150-168 µg/ml), and antiprotein glycation (145-170 µg/ml) as well as antiamylase (216-230 µg/ml), and antiglucosidase (212-238 µg/ml) activity. The essential oils strongly improved the antioxidant capacity of the gelatin-pectin composite so strongly which can be recommended as a natural compound for oxidative stress management.