The enteric glia: identity and functions.

Enteric glial cells were first described at the end of the 19th century, but they attracted more interest from researchers only in the last decades of the 20th. Although, they have a different embryological origin, the enteric GLIA share many characteristics with astrocytes, the main glial cell type of the central nervous system (CNS), such as in their expression of the same markers and in their functions. Here we review the construction of the enteric nervous system (ENS), with a focus on enteric glia, and also the main studies that have revealed the action of enteric glia in different aspects of gastrointestinal tract homeostasis, such as in the intestinal barrier, in communications with neurons, and in their action as progenitor cells. We also discuss recent discoveries about the roles of enteric glia in different disorders that affect the ENS, such as degenerative pathologies including Parkinson's and prion diseases, and in cases of intestinal diseases and injury.

S-nitrosoglutathione decreases inflammation and bone resorption in experimental periodontitis in rats.

BACKGROUND: S-nitrosoglutathione (GSNO) is a nitric oxide donor that may exert antioxidant, anti-inflammatory, and microbicidal actions and is thus a potential drug for the topical treatment of periodontitis. In this study, the effect of intragingival injections of GSNO-containing polyvinylpyrrolidone (PVP) formulations is evaluated in a rat model of periodontitis. METHODS: Periodontal disease was induced by placing a sterilized nylon (000) thread ligature around the cervix of the second left upper molar of the animals, which received intragingival injections of PVP; saline; or PVP/GSNO solutions which corresponded to GSNO doses of 25, 100, and 500 nmol; 1 hour before periodontitis induction, and thereafter, daily for 11 days. RESULTS: PVP/GSNO formulations at doses of 25 and/or 100, but not 500 nmol caused significant inhibition of alveolar bone loss, increase of bone alkaline phosphatase, decrease of myeloperoxidase activity, as well as significant reduction of inflammatory and oxidative stress markers when compared to saline and PVP groups. These effects were also associated with a decrease of matrix metalloproteinases 1 and 8, inducible nitric oxide synthase, and nuclear factor-κB immunostaining in the periodontium. CONCLUSION: Local intragingival injections of GSNO reduces inflammation and bone loss in experimental periodontal disease.

Experimental model of zymosan-induced arthritis in the rat temporomandibular joint: role of nitric oxide and neutrophils.

AIMS: To establish a new model of zymosan-induced temporomandibular joint (TMJ) arthritis in the rat and to investigate the role of nitric oxide. METHODS: Inflammation was induced by an intra-articular injection of zymosan into the left TMJ. Mechanical hypernociception, cell influx, vascular permeability, myeloperoxidase activity, nitrite levels, and histological changes were measured in TMJ lavages or tissues at selected time points. These parameters were also evaluated after treatment with the nitric oxide synthase (NOS) inhibitors L-NAME or 1400 W. RESULTS: Zymosan-induced TMJ arthritis caused a time-dependent leucocyte migration, plasma extravasation, mechanical hypernociception, and neutrophil accumulation between 4 and 24 h. TMJ immunohistochemical analyses showed increased inducible NOS expression. Treatment with L-NAME or 1400 W inhibited these parameters. CONCLUSION: Zymosan-induced TMJ arthritis is a reproducible model that may be used to assess both the mechanisms underlying TMJ inflammation and the potential tools for therapies. Nitric oxide may participate in the inflammatory temporomandibular dysfunction mechanisms.

Lipopolysaccharide from Escherichia coli prevents indomethacin-induced gastric damage in rats: role of non-protein sulfhydryl groups and leukocyte adherence.

OBJECTIVE AND DESIGN: To investigate the role of non-protein sulfhydryl groups (NP-SH) and leukocyte adhesion in the protective effect of lipopolysaccharide (LPS) from Escherichia coli against indomethacin-induced gastropathy. MATERIALS OR SUBJECTS: Male Wistar rats were divided into four groups: saline, LPS, saline + indomethacin and LPS + indomethacin, with six rats in each group. TREATMENT: Rats were pretreated with LPS (300 microg/kg, by intravenous) or saline. After 6 h, indomethacin was administered (20 mg/kg, by gavage). METHODS: Three hours after treatments, rats were killed. Macroscopic gastric damage, gastric NP-SH concentration, myeloperoxidase (MPO) activity and mesenteric leukocyte adhesion (intravital microscopy) were assessed. Statistical analysis was performed using one-way analysis of variance followed by the Newman-Keuls test. Statistical significance was set at P < 0.05. RESULTS: LPS reduced the gastric damage, gastric MPO activity and increased gastric NP-SH concentration in indomethacin-induced gastropathy. LPS alone increased gastric NP-SH when compared to saline. Indomethacin increased leukocyte adhesion when compared to the saline, and LPS reduced indomethacin-induced leukocyte adhesion. In addition, LPS alone did not change leukocyte adhesion, when compared to the saline. CONCLUSION: LPS protective effect against indomethacin-induced gastropathy is mediated by an increase in the NP-SH and a decrease in leukocyte-endothelial adhesion.

Efeito protetor da via hemeoxigenase 1/Biliverdina/CO em modelos de lesões gástricas em camundongos [manuscrito]: papel da guanilato ciclase solúvel (GCS) e da sintase (NOS) / Protective effect track hemeoxigenase 1 / biliverdin / CO in models of gastric lesions in mice [manuscript]: role of soluble guanylate cyclase (GCS) and synthase (NOS)

Avaliar o efeito protetor da via hemeoxigenase 1 (HO-1)/ biliverdina/ CO em modelos de gastropatia em camundongos e o papel da guanilato ciclase solúvel (GCs) e da NOS constitutiva neste evento. Métodos: Protocolo 1: Camundongos foram pré-tratados hemina (indutor da HO-1; 1,3 ou 10mg/kg, i.p.), biliverdina (produto da HO-1; 1,3 ou 1mmg/kg, i.p.), DMDC (doador de CO; 2,5, 7,5, 12,5 ou 25 μmol;kg, i.p.) ou ZnPP I (inibidor da HO-1; 0,3, 1,0 ou 3,0 mg/kg, i.p.) uma hora antes da administração por gavagem de etanol 50% (hemina, biliverdina, DMDC) ou 25% (ZnPP IX). Em outro grupo, os animais foram pré-tratados com ODQ (12,5 mg/kg, v.o.) ou L-NAME (3 mg/kg, v.o.), trinta minutos antes dos tratamentos citados anteriormente. Depois de 1h, os camundongos foram sacrificados e os estômagos removidos para avaliação das lesões gástricas (Image J). Protocolo 2: Camundongos foram pré-tratados hemina (3,0 mg/kg), biliverdina (3,0 mg/kg), DMDC (12,5 μmol/kg) ou ZnPP IX (3,0 mg/kg) uma hora antes da administração de INDO 30 mg/kg (hemina, biliverdina, DMDC) ou 10 mg/kg (ZnPP IX). Em outro grupo os animais foram pré-tratados com ODQ (12,5 mg/kg, v.o.) ou L-NAME (3 mg/kg, v.o.), trinta minutos antes dos tratamentos citados anteriormente. Três horas depois, os camundongos foram sacrificados e os estômagos removidos para avaliação das lesões gástricas, utilizando um paquímetro digital...