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J Neuroimmunol. 2009 Aug 18;213(1-2):20-5. doi: 10.1016/j.jneuroim.2009.05.019. Epub 2009 Jun 28.

Pegylated nanoliposomes remote-loaded with the antioxidant tempamine ameliorate experimental autoimmune encephalomyelitis.

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Laboratory of Membrane and Liposome Research, Department of Biochemistry, The Hebrew University-Hadassah Medical School, Jerusalem, Israel.


Reactive oxygen species are involved in the pathogenesis of multiple sclerosis (MS), Parkinson's disease and neurodegenerative diseases. Here we report that Tempamine (TMN), a stable radical with antioxidant and proapoptotic activities, when encapsulated in the intraliposome aqueous phase of pegylated (<100 nm) nanoliposomes (nSSL), is efficient in inhibiting experimental autoimmune encephalomyelitis (EAE) in mice. The TMN is remote-loaded into nSSL by an intraliposome high/extraliposome low transmembrane ammonium sulfate gradient. Biodistribution studies of nSSL-TMN labeled with the liposome non transferable non metabolizable (3)H-cholesteryl hexadecyl ether show that almost 3% of the injected dose of liposomes reached the brain of the EAE mice, compared with less than 1% in the control healthy mice. This accumulation in the brain, combined with the fact that TMN demonstrates a controlled slow release out of the nSSL, may explain the superior therapeutic activity of nSSL-TMN over free TMN. Our results suggest that the study of nSSL-TMN for therapy of MS, and other neurodegenerative diseases involving oxidative damage, is worth pursuing.

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