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    Comprehensive Metabolite Profiling of Berdav Propolis Using LC-MS/MS: Determination of Antioxidant, Anticholinergic, Antiglaucoma, and Antidiabetic Effects
    (Mdpi, 2023) Karagecili, Hasan; Yilmaz, Mustafa Abdullah; Erturk, Adem; Kiziltas, Hatice; Guven, Leyla; Alwasel, Saleh H.; Gulcin, Ilhami
    Propolis is a complex natural compound that honeybees obtain from plants and contributes to hive safety. It is rich in phenolic and flavonoid compounds, which contain antioxidant, antimicrobial, and anticancer properties. In this study, the chemical composition and antioxidant activities of propolis were investigated; ABTS(center dot+), DPPH center dot and DMPD center dot+ were prepared using radical scavenging antioxidant methods. The phenolic and flavonoid contents of propolis were 53 mg of gallic acid equivalent (GAE)/g and 170.164 mg of quercetin equivalent (QE)/g, respectively. The ferric ion (Fe3+) reduction, CUPRAC and FRAP reduction capacities were also studied. The antioxidant and reducing capacities of propolis were compared with those of butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT), alpha-tocopherol and Trolox reference standards. The half maximal inhibition concentration (IC50) values of propolis for ABTS(center dot+), DPPH center dot and DMPD center dot+ scavenging activities were found to be 8.15, 20.55 and 86.64 mu g/mL, respectively. Propolis extract demonstrated IC50 values of 3.7, 3.4 and 19.6 mu g/mL against alpha-glycosidase, acetylcholinesterase (AChE) and carbonic anhydrase II (hCA II) enzyme, respectively. These enzymes' inhibition was associated with diabetes, Alzheimer's disease (AD) and glaucoma. The reducing power, antioxidant activity and enzyme inhibition capacity of propolis extract were comparable to those demonstrated by the standards. Twenty-eight phenolic compounds, including acacetin, caffeic acid, p-coumaric acid, naringenin, chrysin, quinic acid, quercetin, and ferulic acid, were determined by LC-MS/MS to be major organic compounds in propolis. The polyphenolic antioxidant-rich content of the ethanol extract of propolis appears to be a natural product that can be used in the treatment of diabetes, AD, glaucoma, epilepsy, and cancerous diseases.
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    Öğe
    Hamamelitannin's Antioxidant Effect and Its Inhibition Capability on ?-Glycosidase, Carbonic Anhydrase, Acetylcholinesterase, and Butyrylcholinesterase Enzymes
    (Mdpi, 2024) Durmaz, Lokman; Karagecili, Hasan; Erturk, Adem; Ozden, Eda Mehtap; Taslimi, Parham; Alwasel, Saleh; Gulcin, Ilhami
    Hamamelitannin (2 ',5-di-O-galloyl-hamamelose) bears two-gallate moieties in its structure, and is a natural phenolic product in the leaves and the bark of Hamamelis virginiana. The antioxidant capacity of hamamelitannin was evaluated by a range of methods, with the following findings: the ability to reduce potassium ferric cyanide; the scavenging of N,N-dimethyl-p-phenylenediamine dihydrochloride radical (DMPD center dot+); the scavenging of 2,2 '-azinobis-(3-ethylbenzothiazoline-6-sulphonate) radical (ABTS center dot+); the scavenging of 1,1-diphenyl-2-picrylhydrazyl radical (DPPH center dot); and the ability to reduce cupric ions (Cu2+). Additionally, reference antioxidants of alpha-Tocopherol, butylated hydroxyanisole (BHA), Trolox, and butylated hydroxytoluene (BHT) were used for comparison. For DPPH radical scavenging, hamamelitannin had an IC50 value of 19.31 mu g/mL, while the IC50 values for BHA, BHT, Trolox, and alpha-Tocopherol were 10.10, 25.95, 7.05, and 11.31 mu g/mL, respectively. The study found that hamamelitannin functioned similarly to BHA, alpha-tocopherol, and Trolox in terms of DPPH center dot scavenging, but better than BHT. Additionally, as a polyphenolic secondary metabolite, the hamamelitannin inhibition capability of several metabolic enzymes was demonstrated, including acetylcholinesterase (AChE), butyrylcholinesterase (BChE), carbonic anhydrase I (CA I), carbonic anhydrase II (CA II) and alpha-glycosidase. The Ki values of hamamelitannin exhibited 7.40, 1.99, 10.18, 18.26, and 25.79 nM toward AChE, BChE, hCA I, hCA II, and alpha-glycosidase, respectively.