The objective of this work was to investigate the antidiabetic, antiglycation, and antioxidant potentials of ethanolic extract of seeds of Brazilian Passiflora edulis fruits (PESE), a major by-product of the juice industry, and piceatannol (PIC), one of the main phytochemicals of PESE. PESE, PIC, and acarbose (ACB) exhibited IC50 for alpha-amylase, 32.1 ± 2.7, 85.4 ± 0.7, and 0.4 ± 0.1 µg/mL, respectively, and IC50 for alpha-glucosidase, 76.2 ± 1.9, 20.4 ± 7.6, and 252 ± 4.5 µg/mL, respectively. The IC50 of PESE, PIC, and sitagliptin (STG) for dipeptidyl-peptidase-4 (DPP-4) was 71.1 ± 2.6, 1137 ± 120, and 0.005 ± 0.001 µg/mL, respectively. PESE and PIC inhibited the formation of advanced glycation end-products (AGE) with IC50 of 366 ± 1.9 and 360 ± 9.1 µg/mL for the initial stage and 51.5 ± 1.4 and 67.4 ± 4.6 µg/mL for the intermediate stage of glycation, respectively. Additionally, PESE and PIC inhibited the formation of β-amyloid fibrils in vitro up to 100%. IC50 values for 1,1-diphenyl-2-picrylhydrazyl radical (DPPH•) scavenging activity of PESE and PIC were 20.4 ± 2.1, and 6.3 ± 1.3 µg/mL, respectively. IC50 values for scavenging hypochlorous acid (HOCl) were similar in PESE, PIC, and quercetin (QCT) with values of 1.7 ± 0.3, 1.2 ± 0.5, and 1.9 ± 0.3 µg/mL, respectively. PESE had no cytotoxicity to the human normal bronchial epithelial (BEAS-2B), and alpha mouse liver (AML-12) cells up to 100 and 50 µg/mL, respectively. However, 10 µg/mL of the extract was cytotoxic to non-malignant breast epithelial cells (MCF-10A). PESE and PIC were found to be capable of protecting cultured human cells from the oxidative stress caused by the carcinogen NNKOAc at 100 µM. The in vitro evidence of the inhibition of alpha-amylase, alpha-glucosidase, and DPP-4 enzymes as well as antioxidant and antiglycation activities, warrants further investigation of the antidiabetic potential of P. edulis seeds and PIC.
Shrimps fishing, especially the pink (Farfantepenaeus brasiliensis and F. subtilis) and the white (Litopenaeus schmitti) ones, are relevant for the Brazilian Northeast economy, and their price depends on their aspect-quality. They are rich in lipids/proteins, which are a target for autolytic and microbial enzymes. These may not change the shrimps' appearance but generate substances that may cause poisoning, as histamines. This work compared the microbial quality of fillets and shells of these three shrimps, harvested in two years, after cooking and storage under different freezing times (0-90 days), as well as the total carotenoids (TC) and antioxidant activity (AA%) of ethanolic extracts from all the samples, using spectrophotometry and DPPH test. None histaminogenic and few mesophilic bacteria were isolated (all Gram+ species of Corynebacterium, Listeria, Arthrobacter, Bacillus and Erysipelothrix), but in lower number than the tolerability limit. The TC and AA% of fresh shells from time "zero" were always higher than those of fillets, mainly for F. subtilis. Cooking increased TC and AA% of fillets, but reduced them in shells, and both parameters declined along the freezing. Thin-layer chromatography and spectrophotometric scanning of all the extracts and standards evidenced astaxanthin as the main carotenoid.
This work aimed to investigate the antidiabetic, antiglycation, and antioxidant potentials of the ethanol extract of seeds of Passiflora cincinnata (EPCIN) in vitro. The EPCIN was evaluated from the following assays: total phenolic content (TPC – mg of Gallic Acid Equivalents (GAE)/g of dry extract), Radical Scavenging Assays (DPPH•, HOCl-scavenging assay), and protective effects against glycation of bovine serum albumin (BSA) with methylglyoxal (MGO) or a mixture of reducing sugars, fructose and glucose, as well as the potential for MGO capture by derivatization with ortho-phenylenediamine (OPD). To evaluate the antidiabetic activity of EPCIN in vitro, we used the assays of enzymes α-amylase (4 U/mL), α-glucosidase (0.25 U/mL), and dipeptidyl peptidase-4 (DPP-4 – 3.125 mU). The cell viability of EPCIN-pretreated normal human bronchial epithelial cells (BEAS-2B) alone or in the presence of the carcinogen 4-[(acetoxymethyl)nitrosamine]-1-(3-pyridyl)-1-butanone (NNKOAc) was measured using MTS assay. Quercetin (QCT), piceatannol (PIC), acarbose (ACB), and sitagliptin (STG) were used for comparison purposes. EPCIN had an average of TPC 157.0 ± 1.5 mg of GAE/g of dry extract, exhibited IC50 for DPPH• and HOCl of 11.9 ± 1.8 μg/mL and 6.9 ± 0.9 μg/mL, respectively. EPCIN and AMG inhibited the formation of advanced glycation end-products (AGE) with IC50 of 574 ± 8.7 and 31.9 ± 2.7 μg/mL for the initial stage and 542.6 ± 2.7 and 52.8 ± 8.1 μg/mL for the intermediate stage of glycation, respectively. EPCIN showed IC50 for α-amylase and α-glucosidase of 218.2 ± 15.9 μg/mL (p<0,05) and 242.0 ± 25 μg/mL (p<0,05), respectively. EPCIN did not show cytotoxicity for BEAS-2B cells at 10 and 50 μg/mL concentrations. In addition, it was also able to protect cultured human cells from oxidative stress caused by the NNKOAc at100 μM. The in vitro evidence of the potential antioxidant, antiglycant, and antidiabetic effects warrants further investigation of the antidiabetic potential of Passiflora cincinnata seeds.
This work aimed to investigate the antidiabetic, antiglycation, and antioxidant potentials of the ethanol extract of seeds of Passiflora cincinnata (EPCIN) in vitro. The EPCIN was evaluated from the following assays: total phenolic content (TPC – mg of Gallic Acid Equivalents (GAE)/g of dry extract), Radical Scavenging Assays (DPPH•, HOCl-scavenging assay), and protective effects against glycation of bovine serum albumin (BSA) with methylglyoxal (MGO) or a mixture of reducing sugars, fructose and glucose, as well as the potential for MGO capture by derivatization with ortho-phenylenediamine (OPD). To evaluate the antidiabetic activity of EPCIN in vitro, we used the assays of enzymes α-amylase (4 U/mL), α-glucosidase (0.25 U/mL), and dipeptidyl peptidase-4 (DPP-4 – 3.125 mU). The cell viability of EPCIN-pretreated normal human bronchial epithelial cells (BEAS-2B) alone or in the presence of the carcinogen 4-[(acetoxymethyl)nitrosamine]-1-(3-pyridyl)-1-butanone (NNKOAc) was measured using MTS assay. Quercetin (QCT), piceatannol (PIC), acarbose (ACB), and sitagliptin (STG) were used for comparison purposes. EPCIN had an average of TPC 157.0 ± 1.5 mg of GAE/g of dry extract, exhibited IC50 for DPPH• and HOCl of 11.9 ± 1.8 μg/mL and 6.9 ± 0.9 μg/mL, respectively. EPCIN and AMG inhibited the formation of advanced glycation end-products (AGE) with IC50 of 574 ± 8.7 and 31.9 ± 2.7 μg/mL for the initial stage and 542.6 ± 2.7 and 52.8 ± 8.1 μg/mL for the intermediate stage of glycation, respectively. EPCIN showed IC50 for α-amylase and α-glucosidase of 218.2 ± 15.9 μg/mL (p<0,05) and 242.0 ± 25 μg/mL (p<0,05), respectively. EPCIN did not show cytotoxicity for BEAS-2B cells at 10 and 50 μg/mL concentrations. In addition, it was also able to protect cultured human cells from oxidative stress caused by the NNKOAc at 100 μM. The in vitro evidence of the potential antioxidant, antiglycant, and antidiabetic effects warrants further investigation of the antidiabetic potential of Passiflora cincinnata seeds.
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