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Polyphenols from green tea prevent antineuritogenic action of Nogo-A via 67-kDa laminin receptor and hydrogen peroxide
Usha Gundimeda1, Thomas H. McNeill1, Barsegh A. Barseghian1, William Tzeng1, David Rayudu1, Enrique Cadenas2 and Rayudu Gopalakrishna1,* DOI: 10.1111/jnc.12964Abstract
Axonal regeneration after injury
to the CNS is hampered by myelin-derived inhibitors, such as Nogo-A.
Natural products, such as green tea, which are neuroprotective and safe
for long-term therapy, would complement ongoing various pharmacological
approaches. In this study, using nerve growth factor-differentiated
neuronal-like Neuroscreen-1 cells, we show that extremely low
concentrations of unfractionated green tea polyphenol mixture (GTPP) and
its active ingredient, epigallocatechin-3-gallate (EGCG), prevent both
the neurite outgrowth-inhibiting activity and growth cone-collapsing
activity of Nogo-66 (C-terminal domain of Nogo-A). Furthermore, a
synergistic interaction was observed among GTPP constituents. This
preventive effect was dependent on 67-kDa laminin receptor (67LR) to
which EGCG binds with high affinity. The antioxidants N-acetylcysteine
and cell-permeable catalase abolished this preventive effect of GTPP and
EGCG, suggesting the involvement of sublethal levels of H2O2 in this process. Accordingly, exogenous sublethal concentrations of H2O2,
added as a bolus dose (5 μM) or more effectively through a steady-state
generation (1-2 μM), mimicked GTPP in counteracting the action of
Nogo-66. Exogenous H2O2 mediated this action by
bypassing the requirement of 67LR.
Taken together, these results show for the first time that GTPP and EGCG, acting through 67LR and elevating intracellular sublethal levels of H2O2, inhibit the antineuritogenic action of Nogo-A.
Taken together, these results show for the first time that GTPP and EGCG, acting through 67LR and elevating intracellular sublethal levels of H2O2, inhibit the antineuritogenic action of Nogo-A.
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