Abstract
BackgroundOxidative 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.ResultsIn 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.ConclusionsThe present evidence indicated that EGCG can reduce NADPH-d/nNOS reactivity and thus may enhance motor neuron survival time following peripheral nerve injury.
Highlights
Oxidative stress and large amounts of nitric oxide (NO) have been implicated in the pathophysiology of neuronal injury and neurodegenerative disease
Nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d)/neuronal nitric oxide synthase (nNOS) colocalization studies Labeling for both nNOS and nicotinamide adenine dinucleotide phosphate (NADPH)-d showed that the majority of the NADPH-d positive neurons in the hypoglossal nucleus (HN) and dorsal motor nucleus (DMN) were positive for nNOS (Figure 1)
No NADPH-d and nNOS positive neurons were detected in the HN or the DMN of negative control rats
Summary
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. First identified as the endothelium-derived relaxing factor [5,6], nitric oxide is a short-lived free radical and gaseous biological messenger produced by nitric oxide synthase (NOS) This enzyme catalyzes the oxidation of L-arginine and nicotinamide adenine dinucleotide phosphate (NADPH) by O2. Green tea (Camellia sinensis) is one of the most popular beverages in the world because of its attractive flavor and aroma It contains an abundance of so-called ‘green tea polyphenols (GTPs), typically flavonoids or catechins, which are polyphenolic complexes with potential free radical scavenger activity.
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