Luteolin: Natural Occurrences, Therapeutic Applications and by Alexis J. Dwight

By Alexis J. Dwight

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2. Liver Cancer Numerous studies have demonstrated that luteolin inhibit the cell proliferation and tumor growth in liver cancers. Cell proliferation of liver cancer cell lines SMMC-7721 and BEL-7402 were inhibited by luteolin with dose-time-dependent manner. Luteolin could arrest the cells at G1/S stage, reduce mitochondrial membrane potential, and induce higher apoptosis rate and the typical apoptotic morphological changes of the liver carcinoma cells, and the mechanism maybe through enhancing Bax level, reducing antiapoptotic protein Bcl-2 level, resulting in activating caspase-3 enzyme and decrease of mitochondrial membrane potential, and finally leading to cell apoptosis [65].

In addition, NO can inhibit mitochondria function and break singlestranded DNA. Moreover, NO and superoxide radicals can rapidly combine to form a strong reactive metabolite, peroxynitrite, which is a potent oxidant that can potentially cause membrane lipid peroxidation and lead to myocardial dysfunction [156, 157]. Liao et al. had reported that luteolin also downregulated inducible NO synthase protein and mRNA expression, but did not significantly alter neuronal NO synthase or endothelial NO synthase expression.

Oxidative stress has been reevaluated as an important etiological event implicated in life threatening arrhythmias [183,184]. In addition, evidence suggests that oxidative stress, which is caused by the over-accumulation of intracellular ROS, is one of the leading factors triggering myocyte apoptosis [185]. Myocyte apoptosis can largely induce the development of the myocardial injury [186]. Hence, the modulation of intracellular ROS levels and regulation of apoptotic cascade are considered crucial therapeutic strategies for treating cardiovascular diseases.

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