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This study aims to investigate the protective role of crocetin, a natural antioxidant, against cytotoxicity produced by exposure to norepinephrine (NE) in primary cultured rat cardiac myocytes. Reactive oxygen species (ROS) and Ca(2+) in cells were evaluated by fluorescence microplate reader using 6-carboxy-2',7'-dichlorofluorescein and fluoro-3-acetoxymethyl ester, respectively. Lipid peroxidation was quantified using thiobarbituric acid-reactive substances. The activities of superoxide dismutase (SOD) and contents of glutathione (GSH) were detected by xanthine/xanthime oxidase-mediated ferricytochrome c reduction assay, and recycling effection of glutathione disulfide with GSH reductase and NADPH, respectively. The apoptotic cells were assayed by fluorescein diacetate (FDA)-ethidium bromide (EB) two-staining method. Intracellular accumulation of ROS, Ca(2+), and products of lipid peroxidation resulting from NE were significantly reduced by crocetin. Preincubation of primary cultured rat cardiac myocytes with crocetin remarkably prevented the decrease in SOD activity and quantities of GSH induced by NE. The percentage of NE-induced apoptosis in the cells was decreased by FDA-EB two-staining assay after pretreated with crocetin. The results showed that crocetin may ameliorate NE-induced injury in cardiac myocytes by enhanced SOD activity and increased quantities of GSH, decreased lipid peroxidation and Ca(2+) in cells, and apoptosis death ratio that may represent the cellular mechanisms for its cardioprotective role.

Crocetin, a carotenoid isolated from the Chinese herbal medicine Crocus sativus L. (Saffron), has been shown to have cardiovascular protective effects. The present study investigated the protective action of the antioxidant crocetin against cardiac hypertrophy induced by norepinephrine (NE). This was evaluated by assaying for pathological histological changes with an optical microscope and cell image analysis system. Lipid peroxidation was quantified using thiobarbituric acid-reactive substances (TBARS). Myocardial superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and myocardial catalase (CAT) activities were assayed to evaluate the antioxidant capacity. After long term treatment with NE, antioxidant enzymatic activities were significantly decreased, while products of lipid peroxidation increased. Crocetin markedly reduced the content of lipid peroxidation (LPO), increased the GSH-Px and SOD activity in cardiac hypertrophy, and significantly improved the myocardial pathological histological changes induced by NE. These results suggest that the cardioprotective effects of crocetin are related to modulation of endogenous antioxidant enzymatic activities. Comparing crocetin with captopril, our results indicated that antioxidant activity is an important factor in the therapy of cardiac hypertrophy, but as an antioxidant only, its effects may be limited.

Abstract: Antioxidants have been expected to have potential as antiatherogenic agents. Crocetin is a natural carotenoid antioxidant isolated from Gardenia jasminoids Ellis. Therefore, in the present study, we investigated the inhibitory effect of Crocetin on experimental atherosclerosis in quails. The atherosclerosis model was established by feeding hyperlipidamic diet to quail and Crocetin (25, 50, 100 mg/kg/day) was administered by oral gavage. At the 9th week, serum lipids, malondialdehyde and nitric oxide were measured, and Hematoxylin–Eosin (H&E) stains was used to investigate the histopathological changes of aorta. Results showed that Crocetin could reduce the levels of serum total cholesterol, triglyceride, low density lipoprotein cholesterol and inhibit the formation of aortic plaque. Crocetin could also reduce malondialdehyde and inhibit the descending of nitric oxide in serum. The results suggested that Crocetin could inhibit the formation of atherosclerosis in quails, which might be related to the hypolipidemic effects along with the antioxidative properties of Crocetin. [Copyright &y& Elsevier]