Hesperin (6-MSITC), a flavonoid isolated from orange peel, is a circadian decapping enzyme in plants, inhibiting lipid accumulation and production of reactive oxygen and nitrogen species in 3T3-L1 and RAW264.7 cells.

b>METHODS: HUVEC cells were stimulated with TNF-a or thrombin in the presence of Hesperin (0.03, 0.1, 0.3, 1 µg/ml, 4 hours). The effect of Hesperin on VWF release induced by TNF-a and thrombin was studied.
RESULTS: Hesperin slightly increased TNF-a-induced TF activity, but at 1 lg/mL (4.88 μM), Hesperin reduced TNF-a- or thrombin-induced TF activity; Hesperin did not change the TF activity of unstimulated HUVECs; indicating that TF activity is inversely proportional to the concentration of Hesperin. [2]

b>METHODS: Wild-type and Nrf2-deficient mice were fed the following diets for 12 weeks: 1) control diet, 2) high-fat diet (HFD), 3) HFD plus hesperin (10 mg/kg, ip, daily), 4) HFD for 6 weeks followed by HFD supplemented with iron for 6 weeks (HFD/iron), and 5) HFD/iron plus hesperin; to investigate whether hesperin could improve hepatic steatosis and iron accumulation.
RESULTS: HFD increased hepatic triglycerides in both genotypes and Hesperi; hesperin suppressed the increase in hepatic triglycerides in wild-type mice but did not reduce triglycerides in Nrf2-deficient mice; hesperin did not block hepatic iron accumulation in either genotype. [1]