Phyllanthus amarus does not affect hypernociception in experimental autoimmune encephalomyelitis.

Multiple sclerosis is an inflammatory disease of the central nervous system. Chronic pain is one of the main symptoms, affecting many patients. Studies show that the lignans or the apolar extracts of Phyllanthus amarus have antinociceptive effects in different animal models. To evaluate the antihypernociceptive effect of a hexanic extract of P. amarus in experimental autoimmune encephalomyelitis in mice, the chemical composition of the hexanic extract was analyzed by gas chromatography mass spectrometry. After EAE induction, animals were treated with the hexanic extract of P. amarus for 26 consecutive days. Motor coordination and mechanical hypernociception were evaluated on alternate days. The principal lignans found were phyllanthin, niranthin, and 5-demethoxyniranthin. The hexanic extract of P. amarus at a dose of 100, 200, or 400 mg/kg did not affect the development of the disease. The motor coordination and pain threshold of the treated animals were not altered in this experiment. In conclusion, in this test, the hexanic extract of P. amarus did not show evidence of antihypernociceptive activity in experimental autoimmune encephalomyelitis.

The GABAergic system contributes to the anxiolytic-like effect of essential oil from Cymbopogon citratus (lemongrass).

ETHNOPHARMACOLOGICAL RELEVANCE: The essential oil (EO) from Cymbopogon citratus (DC) Stapf is reported to have a wide range of biological activities and is widely used in traditional medicine as an infusion or decoction. However, despite this widely use, there are few controlled studies confirming its biological activity in central nervous system. MATERIALS AND METHODS: The anxiolytic-like activity of the EO was investigated in light/dark box (LDB) and marble-burying test (MBT) and the antidepressant activity was investigated in forced-swimming test (FST) in mice. Flumazenil, a competitive antagonist of benzodiazepine binding and the selective 5-HT(1A) receptor antagonist WAY100635 was used in experimental procedures to determine the action mechanism of EO. To exclude any false positive results in experimental procedures, mice were submitted to the rota-rod test. We also quantified some neurotransmitters at specific brain regions after EO oral acute treatment. RESULTS: The present work found anxiolytic-like activity of the EO at the dose of 10mg/kg in a LDB. Flumazenil, but not WAY100635, was able to reverse the effect of the EO in the LDB, indicating that the EO activity occurs via the GABA(A) receptor-benzodiazepine complex. Only at higher doses did the EO potentiate diethyl-ether-induced sleeping time in mice. In the FST and MBT, EO showed no effect. Finally, the increase in time spent in the light chamber, demonstrated by concomitant treatment with ineffective doses of diazepam (DZP) and the EO, revealed a synergistic effect of the two compounds. The lack of activity after long-term treatment in the LDB test might be related to tolerance induction, even in the DZP-treated group. Furthermore, there were no significant differences between groups after either acute or repeated treatments with the EO in the rota-rod test. Neurochemical evaluation showed no amendments in neurotransmitter levels evaluated in cortex, striatum, pons, and hypothalamus. CONCLUSIONS: The results corroborate the use of Cymbopogon citratus in folk medicine and suggest that the anxiolytic-like effect of its EO is mediated by the GABA(A) receptor-benzodiazepine complex.