Anti-inflammatory assays on the carrageenin-induced edema and scald-induced hyperalgesia in the hindpaw of rats were studied on polysaccharides obtained from the fruit bodies of various fungi (polysaccharide AC, BC: Tremella fuciformis;MEA, MHA, MCW-A, MCW-N: Auricularia auricula-judae; T-2-HN: Dictophora indusiata;G-A: Ganoderma japonicum). The purified polysaccharides MHA, MCW-A, G-A and T-2-HN exhibited a significant inhibitory effect on carrageenin edema. Among these polysaccharides, T-2-HN (partially O-acetylated alpha-D-mannan) also showed the marked inhibitory effect on scald hyperalgesia. We have found that T-2-HN has more potent anti-inflammatory activity than phenylbutazone in the above two inflammatory models. Since the purified polysaccharide is free from protein and lipid, it is clear that anti-inflammatory effect arises from the polysaccharide itself. The polysaccharides (T-2-HN, locust bean gun, xanthan gum) had little effect on the metabolism of arachidonic acid in canine platelets. The mechanism of the anti-inflammatory activity of the polysaccharide remains obscure.

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These results indicate that aniracetam acts more effective when the forced swim stress-induced immobility is accompanied with brain dysfunction that occurs with aging. The antidepressant-like activity of aniracetam, which is probably due to the combined effects of 2-pyrrolidinone and N-anisoyl-GABA, may be mediated by mainly facilitating dopaminergic transmission (dopamine release and dopamine D2 receptor activation) through nicotinic acetylcholine receptor stimulation.

The effects of clorgyline, the MAO-A inhibitor, and lazabemide, the MAO-B inhibitor, on the levels of the hydroxyl radicals appearing in the cerebral ventricles of mice during brain ischemia/reperfusion were examined by using a salicylate trapping method. The amount of hydroxyl radicals formed peaked at 20 min after reperfusion (approximately 150% vs. basal level). The dopamine level markedly increased shortly after the initiation of an ischemic insult and thereafter waned. By contrast, the concentration of 3,4-dihydroxyphenylacetic acid (DOPAC) level decreased during a 40-min period of ischemia, gradually returning to the preischemic basal level upon reperfusion. The ischemia reperfusion-induced hydroxyl radical generation was attenuated by 3 mg/kg of clorgyline and lazabemide. Furthermore, mice pretreated with these MAO inhibitors showed decreased DOPAC levels in comparison with those of their respective vehicle-treated control groups; recovery of the reduced DOPAC level was also delayed. In conclusion, it is likely that both type A and type B MAOs participate in the generation of hydroxyl radicals during brain ischemia/reperfusion. This finding suggests the possible use of MAO inhibitors as neuroprotective agents for treating ischemic injury.

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