Harpephyllum caffrum stimulates glucose uptake, abates redox imbalance and modulates purinergic and

• 作 者: Kolawole A.Olofinsan Ochuko L.Erukainure Beseni K.Brian Md.Shahidul Islam
• 机 构: Department of Biochemistry,School of Life Sciences,University of KwaZulu-Natal,(Westville Campus),Du
• 出 处: 亚太热带生物医学杂志（英文版）
• 发表日期: 2022年1期
• 关键词: Harpephyllum caffrum Antioxidant Oxidative injury Carbohydrate dysmetabolism

Objective: To investigate the antioxidative and antidiabetic effects of Harpephyllum caffrum bark infusion as well as its effects on glucogenic and nucleotide hydrolyzing enzyme activities in FeSO4-induced oxidative stress in rat hepatic tissue.Methods: Harpephyllum caffrum infusion was prepared from dried plant materials (40 g) infused in boiling water (400 mL) for 20 min at room temperature. The antioxidative and inhibitory activities against carbohydrate digestive enzymes of the infusion were determined using established protocols. The liver tissues of rats were used for glucose uptake assay and to evaluate the infusion\'s effect on endogenous antioxidant, glucogenic, and nucleotide hydrolyzing enzyme activities in FeSO4-induced hepatic injury. Results: The Harpephyllum caffrum infusion significantly reduced ferric iron (FRAP) and free radicals (OH? and DPPH) in a dose-dependent manner. It inhibited α-amylase and α-glucosidase activities and increased glucose uptake in hepatic tissues. FeSO4 significantly decreased glutathione concentration, catalase, and superoxide dismutase activities while increasing malondialdehyde level, glycogen phosphorylase, fructose-1,6-bisphosphatase, and adenosine triphosphatase activities. However, treatment with Harpephyllum caffrum infusion reversed FeSO4-induced changes. Characterization of the infusion revealed the presence of catechol, O-pyrocatechuic acid, mequinol, maltol, and glycoside derivatives. Conclusions: The Harpephyllum caffrum infusion demonstrates antidiabetic and antioxidative potentials in in vitro models of type 2 diabetes as depicted by its ability to inhibit carbohydrate digestive enzymes, mitigate oxidative imbalance, and regulate glucogenic and nucleotide hydrolyzing enzyme activities in oxidative hepatic injury.