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.