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RESUMEN Introducción: Aproximadamente, el 20 % de los pacientes con síndrome radicular lumbosacro crónico no responden a las inyecciones epidurales de esteroides. La radiofrecuencia pulsada del ganglio de la raíz dorsal (GRD) es una alternativa terapéutica en ellos. Objetivos: Evaluar el efecto analgésico de la radiofrecuencia pulsada del GRD en pacientes con síndrome radicular lumbosacro crónico, refractario a los esteroides epidurales. Material y método: 31 pacientes con síndrome radicular lumbosacro crónico que no respondieron a dos inyecciones epidurales de esteroides fueron tratados con radiofrecuencia pulsada del GRD a 45 V y 42 °C, en 2 ciclos de 120 segundos. Se utilizó el Inventario Abreviado de Dolor para evaluar los resultados. Se consideró una respuesta satisfactoria al procedimiento una disminución de dos puntos en la escala verbal numérica (EVN) evaluada en la pregunta 6 del inventario abreviado de dolor. Los índices de intensidad y de interferencia fueron calculados antes y después del tratamiento. Resultados: La EVN se redujo de 7,7 ± 2,2 a 5,9 ± 3 (p < 0,01). Los índices de intensidad e interferencia disminuyeron de 7,1 ± 1,5 a 5,9 ± 2,1 (p < 0,01) y 7,1 ± 1,9 a 6,0 ± 2,3 (p < 0,02) respectivamente. 12 de los 30 pacientes (40 %) presentaron una respuesta analgésica satisfactoria. En estos, la EVN disminuyó de 8,0 ± 1,5 a 3,8 ± 2,6 y los índices de intensidad e interferencia de 7,4 ± 1,3 a 3,9 ± 1,5 (p < 0,0001) y 7,7 ± 1,9 a 4,9 ± 2,7 (p = 0,002), respectivamente. Conclusiones: La aplicación de radiofrecuencia pulsada en el GRD reduce en forma discreta pero estadísticamente significativa la intensidad del dolor y su interferencia funcional en pacientes con síndrome radicular lumbosacro refractario a las inyecciones epidurales de esteroides, al mes de realizada. En aproximadamente el 40 % se obtuvieron respuestas analgésicas satisfactorias que, en algunos casos, se extendió a tres meses tras realizar el procedimiento. ABSTRACT Introduction: Approximately 20 % of patients with chronic lumbosacral radicular syndrome do not respond to epidural steroid injections. Pulsed radiofrequency of the dorsal root ganglion (DRG) is proposed as an alternative treatment. Objetive: To evaluate the analgesic effect of pulsed radiofrequency of the DRG in patients with chronic lumbosacral radicular syndrome, refractory to epidural steroid injections. Patients and method: 31 patients with chronic lumbosacral radicular syndrome that failed to at least two epidural steroid injections, received pulsed radiofrequency of the DRG, utilizing two cycles of 120 seconds, 45 V and 42 °C. Evaluation was carried out a month later. Brief Pain Inventory was applied before procedure and one month later. A reduction of 2 points in the verbal numerical scale (VNS) assessed with the question 6 of the Brief Pain Inventory, was considered a satisfactory analgesic response. Intensity and Interference Scores were calculated. Results: The VNS score decreased from 7.7 ± 2,2 to 5.9 ± 3 (p < 0.01). Intensity and Interference Scores were reduced from 7.1 ± 1.5 to 5.9 ± 2.1 (p < 0.01) and 7.1 ± 1.9 to 6.0 ± 2.3 (p < 0.02) respectively. In 12 patients (40 %) a satisfactory analgesic response was observed. In these patients the VNS decreased from 8.0 ± 1.5 to 3.8 ± 2.6. Intensity and Interference Scores were reduced from 7.4 ± 1.3 to 3.9 ± 1.5 (p < 0.0001) y 7.7 ± 1.9 to 4.9 ± 2,7 (p = 0.002) respectively. Conclusions: DRG pulsed radiofrequency produce a mild but statistically significant reduction in VNS and pain interference, in patients with chronic lumbosacral radicular syndrome. However, in 40 % of the patients a satisfactory analgesic effect was observed. In some of them this changes persist after 3 months of the procedures.

We describe herein a new approach to prepare unprecedented bioactive indolizine motifs decorated with organosulfur and organoselenium groups. A total of 12 1-sulfanylindolizines and 2 1-selanylindolizines were prepared in excellent yields by an intramolecular annulation of easily prepared chalcogen-containing pyridinium salts. The reaction is fast (1 h at 70 °C or 5 min under sonication) and transition-metal-free, using glycerol as a green solvent.

Monosodium glutamate (MSG) is a neuroexcitatory amino acid commonly used as flavoring of foods. MSG neonatal administration to animals leads to behavioral and physiological disorders in adulthood, including increased pain sensitivity. This study aimed to investigate the effect of diphenyl diselenide (PhSe)2, an organoselenium compound with pharmacological properties already documented, on nociception induced by MSG. Newborn Wistar rats received 10 subcutaneous injections of MSG at a dose of 4.0g/kg or saline (once daily). At the 60th day of life, the rats were daily treated with (PhSe)2 (1mg/kg) or vehicle (canola oil) by the intragastric route for 7 days. The behavioral tests (locomotor activity, hot plate, tail-immersion and mechanical allodynia) were carried out. Ex vivo assays were performed in samples of hippocampus to determine Na(+), K(+)-ATPase and Ca(2+)-ATPase activities, cytokine levels and [(3)H]glutamate uptake. The results demonstrated that MSG increased nociception in the hot plate test and in the mechanical allodynia stimulated by Von-Frey hair but did not alter the tail immersion test. (PhSe)2 reversed all nociceptive behaviors altered by MSG. MSG caused an increase in Na(+),K(+)-ATPase and Ca(2+)-ATPase activities and in pro-inflammatory cytokine levels and a decrease in the anti-inflammatory cytokine and in the [(3)H]glutamate uptake. (PhSe)2 was effective in reversing all alterations caused by MSG. The results indicate that (PhSe)2 had a potential antinociceptive and anti-inflammatory action in the MSG model.

Objectives This study investigated the involvement of different types of K+ channels and PPARγ receptors in the antidepressant-like effect of diphenyl diselenide in mice. Methods Mice were pretreated with subeffective doses of K+ channel inhibitors (tetraethylammonium, glibenclamide, charybdotoxin and apamin), openers (cromakalim, minoxidil), GW 9662 (a PPARγ antagonist) or vehicle. Thirty minutes later the mice received diphenyl diselenide in either an effective or a subeffective dose, 30 min before a tail-suspension test. Key findings Pre-treatment with tetraethylammonium, charybdotoxin or apamin combined with a subeffective dose of diphenyl diselenide was effective in decreasing the immobility time in the mouse tail-suspension test. The reduction in the immobility time elicited by an effective dose of diphenyl diselenide in this test was prevented by the pretreatment of mice with minoxidil and GW 9662. Conclusions Diphenyl diselenide elicited an antidepressant-like effect and this action was mediated, at least in part, by modulation of K+ channels and PPARγ receptors.

Context: Organoselenium compounds have been described as antioxidant and neuroprotective agents.Objective: To evaluate the antioxidant action of 2,2′-dithienyl diselenide (DTDS) and its effects in brain monoamine oxidase (MAO) activity in vitro.Materials and methods: Assays for reactive species (RS), lipid peroxidation, protein oxidation, MAO A and B activities in rat brain homogenate as well as mimetic dehydroascorbate reductase and glutathione S-transferase activities were performed using DTDS (μM range).Results: DTDS was effective in decreasing the levels of RS as well as lipid peroxidation induced by malonate, sodium nitroprusside or FeCl2/EDTA and protein carbonyl in the rat brain homogenate. DTDS elicited dehydroascorbate reductase-like and glutathione S-transferase-like activities. DTDS was effective in inhibiting both MAO-A and MAO-B activities.Discussion: The results demonstrated that DTDS is an antioxidant agent with non-selective inhibitory effect on MAO activity.Conclusion: DTDS is a promising...

The present study was designed to investigate the effects of p-methoxyl-diphenyl diselenide (OMePhSe)(2) on oxidative stress and renal damage parameters of mice exposed to cisplatin. (OMePhSe)(2) (50 and 100 mg/kg/day) was orally administered to mice for six consecutive days. On the third day after the beginning of (OMePhSe)(2) treatment, the renal toxicity was induced by injecting cisplatin (10 mg/kg intraperitoneal) in mice. (OMePhSe)(2) treatment (50 mg/kg) partially reduced plasma urea and creatinine levels increased by cisplatin. Histopathological examination of kidneys showed that (OMePhSe)(2) ameliorated renal injury caused by cisplatin. (OMePhSe)(2) attenuated the decrease in reduced glutathione (GSH) and ascorbic acid (AA) levels, the inhibition of glutathione peroxidase (GPx), glutathione S-transferase (GST), glutathione reductase (GR) and catalase (CAT) activities caused by cisplatin in kidney. (OMePhSe)(2) treatment partially protected against the inhibition of renal δ-aminolevulinic dehydratase (δ-ALA-D) activity caused by cisplatin. No alteration in renal lipid peroxidation levels was found in cisplatin and/or (OMePhSe)(2) groups. (OMePhSe)(2) was effective against the increase in reactive species (RS) levels caused by the cisplatin exposure. Based on the renoprotective and antioxidant actions of (OMePhSe)(2) we suggest that this organoselenium compound could be considered a feasible candidate to protect against toxicity commonly encountered in cisplatin exposure.