Hesperetin belongs to the flavanone class of flavonoids. Hesperetin, in the form of its glycoside hesperidin, is the predominant flavonoid in lemons and oranges.

Hesperetin在自体纳米乳化药物输送系统中保持了抗氧化潜力[1]。Hesperetin和NGR对人类UGTs表现出广谱抑制作用。此外，Hesperetin对UGT1A1、1A3和1A9表现出强烈的抑制效果（IC50及Ki值均低于10μM），对UGT1A4、UGT1A7、UGT1A8表现出中等抑制（IC50值为29.68-63.87μM）[2]。Hesperetin与不同类型的蛋白质通过氢键、π-π效应、π-阳离子键合和π-σ作用相互作用，绑定能量各不相同。Hesperetin 具有研究 CHIKV感染疗法的潜力[3]。Hesperetin剂量依赖性减少了GCDCA诱导的原代大鼠肝细胞中caspase-3活性。Hesperetin还剂量依赖性减少了CM诱导的肝细胞中Nos2（iNOS）表达。有趣的是，与仅有细胞因子混合物相比，Hesperetin诱导的抗氧化基因血红素加氧酶1（HO-1）表达量大约增加了四倍[5]。

Hesperetin（40 mg/kg b.w., 口服）的预先给药显著减轻了Cd引起的氧化应激和线粒体功能障碍，恢复了大鼠脑中的抗氧化剂和膜结合酶活性，并减少了细胞凋亡[4]。Hesperetin（200 mg/kg）减轻了Con A引起的小鼠肝细胞凋亡和肝脏Nos2（iNOS）的表达。此外，Hesperetin的联合治疗减少了凋亡体、水肿性变性、核碎片、自溶和出血的发生。在以D-GalN/LPS诱导的小鼠急性肝炎模型中，Hesperetin显著减少了肝组织中浸润的白细胞数量[5]。

First, 0.5 mL tissue homogenate is diluted with 1 mL water. Then, to this mixture, 2.5 mL ethanol and 1.5 mL chloroform (all reagents chilled) are added and shaken for 1 min at 4°C, then centrifuged. The enzyme activity in the supernatant is determined. The assay mixture contained 1.2 mL sodium pyrophosphate buffer (0.025 M, pH 8.3), 0.1 mL 186 mM phenazine methosulfate (PMS), 0.3 mL 30 mM Nitroblue tetrazolium (NBT), and 0.2 mL of nicotinamide adenine dinucleotide (NADH), and appropriately diluted enzyme preparation and water in a total volume of 3 mL. Reaction is initiated by the addition of NADH. After incubation at 30°C for 90 min, the reaction is stopped by the addition of 1 mL glacial acetic acid. The reaction mixture is stirred vigorously and shaken with 4 mL n-butanol. The intensity of the chromogen in the butanol layer is measured at 560 nm against a butanol blank. A system without enzyme served as control. One unit of enzyme activity is defined as 50% inhibition of NBT reduction in 1 min under the assay conditions.