Nano-liposomes of lycopene reduces ischemic brain damage in rodents by regulating iron metabolism

Publication date: 20 August 2018
Source:Free Radical Biology and Medicine, Volume 124
Author(s): Yashuo Zhao, Zhen Xin, Nina Li, Shiyang Chang, Yandong Chen, Lina Geng, Hengrui Chang, Honglian Shi, Yan-Zhong Chang
In order to discover new drug delivery approaches and to understand the mechanism of iron overload in cerebral ischemia/reperfusion (I/R), we aimed to investigate the effects of lycopene (LYC) in the form of nano-liposomes (L-LYC) on iron-regulating proteins and ischemic brain injury. We found that L-LYC significantly increased the LYC content in serum and the brain. Adult male Sprague-Dawley rats treated with L-LYC for 14 days were subjected to 60 min of ischemia and 7 days of reperfusion. The effects of L-LYC were evaluated by infarction volume, neurological score, neuronal apoptosis, and markers for oxidative stress. Levels of iron-regulating protein such as hepcidin and ferroportin (FPN1) were examined. L-LYC reduced cerebral infarction and improved neurobehavior of the rats more efficiently than "naked" LYC. L-LYC reduced protein levels of oxidases (e.g. nitric oxide synthase and NOX2), increased the level of Bcl-2, lowered caspase-3, and suppressed apoptosis through inhibiting MAPK-JNK. Furthermore, L-LYC suppressed hepcidin-mediated decrease in FPN1, a sole iron exporter, and normalized the levels of iron. We further demonstrated that the effect of L-LYC on hepcidin expression might result from its ability to attenuate the release of the inflammatory factor interleukin 6. The results demonstrated that nano-liposomal encapsulation significantly improved LYC efficacy in providing neuronal protection against I/R injury. The data also revealed a novel mechanism of L-LYC's neuroprotection by regulating iron metabolism in an ischemic brain.

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