Abstract
(+)-catechin is an active natural substance for hyperglycemia. However, HSA may be affected by high blood glucose, which alters HSA in the secondary structure to affect the combination of (+)-catechin and HSA, resulting in a “traffic jam” of (+)-catechin in the body. In this study, the effect of glucose on the binding between (+)-catechin and HSA was studied by multiple analysis techniques. It was found that glucose could not alter the static quenching of (+)-catechin-HSA. Electrostatic force played an important role through thermodynamics parameters. The binding constants were 4.956 × 105 mol⋅L-1, ΔH° = –33.6 kJ⋅mol−1, and ΔS° = 99.68 J⋅mol−1⋅K−1 in the glucose-free environment and the binding constants were 4.602 × 104 mol⋅L-1, ΔH° = −20.4 kJ⋅mol−1 and ΔS° = 57.7 J⋅mol−1⋅K−1 in the glucose environment at 298 K. We found that the binding sites of (+)-catechin in two environments were site II through the probe test. 3D fluorescence and CD experiments indicated the addition of (+)-catechin changed the secondary structure of HSA. Besides, molecular docking manifested that glucose could affect the combine of HSA and (+)-catechin. (+)-catechin had weaker binding to HSA in the glucose environment, which was different from the combination of (+)-catechin and HSA alone. The dosage of (+)-catechin for diabetic patients should be reduced because the concentration of free (+)-catechin would increase in the body. This study had a certain guiding significance for the medication of diabetic patients.
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