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. 2016 Apr;11(4):545-6.
doi: 10.4103/1673-5374.180729.

Counteraction of Nogo-A and axonal growth inhibitors by green tea polyphenols and other natural products

Tiffany K Fan  1 , Usha Gundimeda  1 , William J Mack  2 , Rayudu Gopalakrishna  1
Affiliations

Counteraction of Nogo-A and axonal growth inhibitors by green tea polyphenols and other natural products

Tiffany K Fan et al. Neural Regen Res. 2016 Apr.
No abstract available

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Figures

Figure 1
Figure 1
Schematic presentation of proposed mechanisms by which GTPP and other natural products counteract Nogo-A and other axonal growth inhibitors. Binding of Nogo-A and other axonal growth inhibitors to NgR1 receptor complex leads to activation of RhoA and its effector, RhoA-associated protein kinase (ROCK). This ultimately leads to reorganization of actin cytoskeleon, causing growth cone collapse and neurite outgrowth inhibition. EGCG binding to its cell-surface receptor leads to activation of NADPH oxidase and an increase in the generation of H2O2 (Gundimeda et al., 2012). Either endogenously generated H2O2 in response to EGCG treatment or exogenous H2O2 alone prevents the antineuritogenic action of Nogo-A (Gundimeda et al., 2015). We hypothesize that H2O2 may accomplish this directly through inhibiting RhoA by either inducing its redox modification or enhancing tyrosine phosphorylation-mediated activation of p190RhoGAP, an endogenous inhibitor of RhoA. Various natural products from Chinese medicines may decrease the expression of Nogo-A and/or NgR1 and enhance axonal regeneration (Qin et al., 2012). Daidzein, a soy isoflavone, blocks the antineuritogenic action of MAG by inducing arginase and polyamine synthesis (Ma et al., 2010). 67LR: 67-kDa laminin receptor; EGCG: epigallocatechin-3-gallate; GTPP: green tea polyphenols; MAG: myelin-associated glycoprotein; NADPH: nicotinamide adenine dinucleotide phosphate; NgR1: Nogo-66 receptor 1; OMgp: oligodendrocyte myelin glycoprotein.
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