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Abstract Purpose Lutein (LUT) is a carotenoid found in fruits, and green vegetables with potent antioxidant, anti-inflammatory and cardioprotective action. However, the mechanisms involved in the cardioprotection against cardiac hypertrophy (CH) remains unkown. Objectives Investigate the anti-hypertrophic action of LUT in rats using the isoproterenol-induced CH model. Methods For CH induction, isoproterenol (ISO; 4.5 mg/kg/day, 7 days, i.p) was administrated and animals were treated with LUT (20 mg/kg/day, 7 days) or apocynin (APO, 10 mg/kg/day, 7 days). To investigate the participation of the nitric oxide (NO) pathway in the mechanism of action of LUT, the animals were treated with L-NAME (20 mg/kg/day, 7 days), an inhibitor of NO synthase. Results LUT and APO animals showed attenuated morphometric, fibrosis and inflammatory enhancement compared to ISO group, in addition to reducing the infarct area and the mortality rate triggered by ISO. Serum levels of CPK-TOTAL, CPK-MB, LDH, AST and ALT were significantly reduced in animals treated with LUT when compared to the ISO group. LUT attenuated the electrocardiographic changes induced by ISO (increase of QRS and QTc and inversion of T wave) and prevented the reduction of left ventricular pressure and heart rate in the ISO group. ISO increased the production of reactive oxygen species (ROS) in the heart which was prevented by LUT. ISO increased the Bax protein expression, which was attenuated by LUT treatment. Also, L-NAME partially reversed the LUT-mediated cardioprotection. Conclusion The results show that LUT exerts a cardioprotective effect against CH in rats partially related to NO pathway.
Santos et al. (Fri,) studied this question.