This present study investigated the antioxidative and antidiabetic properties of kolaviron by analysing its inhibitory effect on key metabolic activities linked to T2D, in vitro and ex vivo. Kolaviron significantly inhibited α-glucosidase and α-amylase activities, and intestinal glucose absorption dose-dependently, while promoting muscle glucose uptake. Induction of oxidative pancreatic injury significantly depleted glutathione level, superoxide dismutase, catalase, and ATPase activities, while elevating malondialdehyde and nitric oxide levels, acetylcholinesterase and chymotrypsin activities. These levels and activities were significantly reversed in tissues treated with kolaviron. Kolaviron depleted oxidative-induced metabolites, with concomitant restoration of oxidative-depleted metabolites. It also inactivated oxidative-induced ascorbate and aldarate metabolism, pentose and glucuronate interconversions, fructose and mannose metabolism, amino sugar and nucleotide sugar metabolism, and arginine and proline metabolism, while reactivating selenocompound metabolism. These results depict the antidiabetic properties of kolaviron as indicated by its ability to attenuate oxidative-induced enzyme activities and dysregulated metabolisms, and modulated the enzyme activities linked to hyperglycaemia.

本研究通过分析其对与T2D相关的关键代谢活性的体外和离体抑制作用，研究了Kolaviron的抗氧化和抗糖尿病特性。。Kolaviron显着抑制α-葡萄糖苷酶和α-淀粉酶的活性，并肠道葡萄糖的吸收呈剂量依赖性，同时促进肌肉对葡萄糖的吸收。氧化性胰腺损伤的诱导显着消耗了谷胱甘肽水平，超氧化物歧化酶，过氧化氢酶和ATPase活性，同时升高了丙二醛和一氧化氮水平，乙酰胆碱酯酶和胰凝乳蛋白酶活性。这些水平和活性在用科拉维龙治疗的组织中显着逆转。Kolaviron消耗了氧化诱导的代谢产物，并同时恢复了氧化消耗的代谢产物。它还使氧化诱导的抗坏血酸和藻酸酯代谢，戊糖和葡萄糖醛酸酯相互转化，果糖和甘露糖代谢，氨基糖和核苷酸糖代谢以及精氨酸和脯氨酸代谢失活，同时激活硒化合物代谢。这些结果描述了kolaviron的抗糖尿病特性，该特性由其减弱氧化诱导的酶活性和代谢失调以及调节与高血糖有关的酶活性的能力所表明。