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(-)-Epigallocatechin gallate attenuates NADPH-d/nNOS expression in motor neurons of rats following peripheral nerve injury

I-Hua Wei1*, Hui-Chin Tu4, Chih-Chia Huang2, Mang-Hung Tsai1, Chi-Yu Tseng3 and Jeng-Yung Shieh4*

Author Affiliations

1 Department of Anatomy and Cell Biology, College of Medicine, China Medical University, Taichung, Taiwan

2 Department of Psychiatry, China Medical University and Hospital, Taichung, Taiwan

3 Department of Neurology, Taichung Tzu Chi General Hospital, Taichung, Taiwan

4 Department of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei, Taiwan

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BMC Neuroscience 2011, 12:52  doi:10.1186/1471-2202-12-52

Published: 1 June 2011



Oxidative stress and large amounts of nitric oxide (NO) have been implicated in the pathophysiology of neuronal injury and neurodegenerative disease. Recent studies have shown that (-)-epigallocatechin gallate (EGCG), one of the green tea polyphenols, has potent antioxidant effects against free radical-mediated lipid peroxidation in ischemia-induced neuronal damage. The purpose of this study was to examine whether EGCG would attenuate neuronal expression of NADPH-d/nNOS in the motor neurons of the lower brainstem following peripheral nerve crush. Thus, young adult rats were treated with EGCG (10, 25, or 50 mg/kg, i.p.) 30 min prior to crushing their hypoglossal and vagus nerves for 30 seconds (left side, at the cervical level). The treatment (pre-crush doses of EGCG) was continued from day 1 to day 6, and the animals were sacrificed on days 3, 7, 14 and 28. Nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry and neuronal nitric oxide synthase (nNOS) immunohistochemistry were used to assess neuronal NADPH-d/nNOS expression in the hypoglossal nucleus and dorsal motor nucleus of the vagus.


In rats treated with high dosages of EGCG (25 or 50 mg/kg), NADPH-d/nNOS reactivity and cell death of the motor neurons were significantly decreased.


The present evidence indicated that EGCG can reduce NADPH-d/nNOS reactivity and thus may enhance motor neuron survival time following peripheral nerve injury.