We have examined the possible protective effects of Polygala paniculata extract against methylmercury (MeHg)-induced neurotoxicity in adult mice. MeHg was diluted in drinking water (40 mg L(-1), freely available) and the hydroalcoholic Polygala extract was diluted in a 150 mM NaCl solution and administered by gavage (100 mg kg(-1) b.w., twice a day). After a two-week treatment, MeHg exposure significantly inhibited glutathione peroxidase and increased glutathione reductase activity, while the levels of thiobarbituric acid reactive substances were increased in the cerebral cortex and cerebellum. These alterations were prevented by administration of Polygala extract, except for glutathione reductase activity, which remained elevated in the cerebral cortex. Behavioural interference in the MeHg-exposed animals was evident through a marked deficit in the motor performance in the rotarod task, which was completely recovered to control levels by Polygala extract co-administration. This study has shown, for the first time, the in-vivo protective effects of Polygala extract against MeHg-induced neurotoxicity. In addition, our findings encourage studies concerning the beneficial effects of P. paniculata on neurological conditions related to excitotoxicity and oxidative stress.

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Cipura paludosa (Iridaceae), a native plant widely distributed in the north of Brazil, is used in traditional medicine as an anti-inflammatory and analgesic agent, against tuberculosis and gonorrhoea and for regulation of menstrual flow. However, scientific studies on the pharmacological properties of C. paludosa are scarce. We have examined the potential protective effects of the ethanolic extract of C. paludosa against methyl mercury (MeHg)-induced neurotoxicity in adult mice. MeHg was diluted in drinking water (40 mg/l, freely available) and the ethanolic C. paludosa extract (CE) was diluted in a 150 mM NaCl solution and administered by gavage (10 and 100 mg/kg body weight, respectively, twice a day). Because treatment lasted for 14 days and each animal weighed around 40 g, the total dosage of plant extract given to each mouse was 5.6 and 56 g, respectively. After the treatment period, MeHg exposure induced a significant deficit in the motor coordination, which was evident by a reduction (90%) in the falling latency in the rotarod apparatus. Interestingly, this phenomenon was completely recovered to control levels by CE co-administration, independent of dosages. MeHg exposure inhibited cerebellar glutathione peroxidase (mean percentage inhibition of 42%) -an important enzyme involved in the detoxification of endogenous peroxides -and this effect was prevented by co-administration of CE. Conversely, MeHg exposure increased cerebellar glutathione reductase activity (mean percentage inhibition of 70%), and this phenomenon was not affected by C. paludosa co-administration. Neither MeHg nor CE changed the cerebellar glutathione levels. This study has shown for the first time, the in vivo protective effects of CE against MeHg-induced neurotoxicity. In addition, our findings encourage studies concerning the beneficial effects of C. paludosa on neurological conditions related to excitotoxicity and oxidative stress.

This study investigated the role of the glutamatergic system on the antinociception caused by Polygala sabulosa hydroalcoholic extract (HE). The systems mediated by substance P, capsaicin, interleukin-1 β (IL-1 β ) and tumour necrosis factor-α (TNF-α ) were also investigated. P. sabulosa HE given orally produced a significant inhibition of glutamateinduced paw licking ) mg/kg and inhibition of 79 ± 6% at 1000 mg/kg]. The plant derivatives α -spinasterol, scopoletin and styryl-2-pyrones (compound 1 and 3) (10 mg/kg, intraperitoneally) inhibited 80 ± 7%, 46 ± 11%, 45 ± 11% and 35 ± 13% the nociceptive response caused by glutamate, respectively. Furthermore, P. sabulosa HE (500 mg/kg, orally) caused marked inhibition of nociceptive response induced by intrathecal injection of glutamate, N-methyl-d -aspartic acid, α -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, kainate, TNF-α and IL-1 β , with inhibitions of 44 ± 7%, 55 ± 4%, 38 ± 10%, 61 ± 7%, 76 ± 9% and 100%, respectively. In contrast, P. sabulosa HE (500 mg/kg, orally) did not affect the biting response induced by the metabotropic glutamatergic receptor agonist (±)-1-aminocyclopentanetrans -1,3-dicarboxylic acid, substance P and capsaicin. The locomotor activity was altered only in mice treated with a very high dose (1000 mg/kg) of P. sabulosa HE. Our results showed that the antinociceptive effects of P. sabulosa HE are associated with an inhibition of glutamatergic transmission and an inhibition of pathways dependent on pro-inflammatory cytokines. The plant derivatives α -spinasterol, scopoletin and styryl-2-pyrones play an important role on the antinociceptive effects of P. sabulosa HE.The plants of genus Polygala are widely distributed in Santa Catarina state, Brazil, and have been employed to treat disorders of the bowel and kidney, as a topical anaesthetic and expectorant [1]. Scientific studies in isolated cells and in animals have confirmed the biological activities of the plants from genus Polygala [2-10]. The chemical constituents of Polygala , coumarins, steroids, saponins, lignans, flavonoids and xanthones confer to these plants valuable pharmacological properties [7][8][9][10][11][12][13].Recently, we have demonstrated that Polygala sabulosa hydroalcoholic extract (HE) A. W. Bennett (Polygalaceae) produced antinociceptive action against the acetic acidinduced visceral nociception. The presence of styryl-2-pyrones, coumarin (scopoletin) and steroid ( α -spinasterol) gives to the plant a potent antinociceptive effect [9]. However, the model of nociception previously employed did not allow to clearly identify the mechanism of the antinociceptive action of the plant extract. Indeed, the acetic acid-induced visceral nociception involves a chain of inflammatory mediators that are released into the abdominal cavity and in the central nervous system [14][15][16].In this concern, the aim of this study was to identify the mechanism by which P. sabulosa HE exerts its antinociceptive effect. For this purpose, the effects of the P. sabulosa HE we...

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