Influence of Prebiotic Activity of Agave salmiana Fructans on Mucus Production and Morphology Changes in Colonic Epithelium Cell of Healthy Wistar Rats.

The beneficial health of evaluating prebiotic effect by the consumption of Agave salmiana fructans (A. salmiana fructans) was assessed in the epithelium of the cecum and proximal colon of Wistar rats fed at different doses for 35 days with regards to mucus production, morphological cell changes, and the serum concentration of tumor necrosis factor-α (TNF-α). Results showed a significant increase in mucus-secreting cells (P < 0.05) and a normal structure with preserved crypts, without morphological damage to colonic cells for a dose of 12.5% (w/w) with respect to the control and the other doses evaluated. The concentration of pro-inflammatory cytokine TNF-α was decreased significantly (P < 0.05) in the groups with doses of 10 and 12.5% (w/w) at 7 and 35 days, respectively. This effect was positively correlated with the reduction of inflammation in epithelial cells. This study provides direct evidence of the effects of the A. salmiana fructans on the colonic epithelium, demonstrating that a diet supplemented with 12.5% of fructans for 35 days exerts health benefits through the strengthening of the mucosa layer, which favors the adherence of the bacterial population and suppresses inflammation.

Anti-inflammatory and anti-oxidant effect of Calea urticifolia lyophilized aqueous extract on lipopolysaccharide-stimulated RAW 264.7 macrophages.

ETHNOPHARMACOLOGICAL RELEVANCE: Calea urticifolia leaves are traditionally used as a remedy to treat gastric ulcers, diabetes, and inflammation by the Xi'uy ancient native community of San Luis Potosi, Mexico. AIM OF THE STUDY: The aim was to assess the effects of the aqueous extract of the Mexican plant C. urticifolia as anti-inflammatory and anti-oxidant using lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages and to provide evidence on the phenolic compounds. MATERIALS AND METHODS: RAW 264.7 macrophages were stimulated with 1µg/mL of LPS and treated with 10, 25 50, 75 y 100µg/mL of Calea urticifolia lyophilized aqueous extract (CuAqE). Nitric oxide (NO) release, tumor necrosis factor alpha, prostaglandin E2 production, inducible nitric oxide synthase (iNOS), cyclooxygenase-2, nuclear factor-κB (NF-κB) p65, NF-κB p50 expression and reactive oxygen species (ROS) were measured; other pro-inflammatory proteins were measured with membrane antibody array. Phenolic compounds were analyzed by LC-ESI-MS. RESULTS: Inflammation was inhibited by suppressing iNOS/NO pathway through inhibiting nucleus translocation of NF-κB p65 and p50 sub-units. ROS production was significantly (P<0.05) inhibited in a dose-dependent manner in LPS-stimulated macrophages. Moreover, the expression of inflammatory markers was suppressed (34.5-88.3%) by CuAqE. A mix of caffeoylquinic acid derivatives and flavonoid-glycosides were found in CuAqE. CONCLUSION: Phenolic compounds in CuAqE such as caffeoylquinic acid derivatives and flavonoid glycosides could be responsible for inhibiting LPS-induced inflammation and oxidative stress by iNOS/NO pathway through suppressing NF-κB signaling pathway and by inhibition of ROS production in RAW 264.7 macrophages. Therefore, these results support the traditional knowledge of C. urticifolia tea such as an anti-inflammatory and antioxidant agent.

Evaluación nutricional en adultos mayores en una Unidad de Medicina Familiar / Nutritional assessment in elderly patients in a Family Medicine Unit

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Functional and morphological effects of repeated sodium arsenite exposure on rat peripheral sensory nerves.

Exposure to inorganic arsenic (iAs) is known to result in peripheral neuropathy. To better understand the functional and morphological consequences of iAs exposure, we examined the electrophysiological and histological characteristics of the sensory sural nerves in adult Male Wistar rats following 30 days of sodium arsenite administration by gavage (10 mg/kg body weight/day). Arsenic (As) levels in the peripheral nerves of exposed animals were about 150 times greater than those in controls. Lipid peroxidation was also increased in iAs-exposed animals. Compound action potentials (CAPs) evoked in iAs-exposed nerves were characterized by a slower conduction velocity ( approximately 26%). iAs-exposed nerves also showed a trend towards a decreased CAP area ( approximately 35%). These electrophysiological changes were consistent with histological alterations such as a approximately 56% decrease in myelin thickness. In addition, the perimeter and transverse area of axons were reduced to 29% and 45% of control, respectively. Our results suggest that accumulation of As produced by iAs exposure induces oxidative damage, severe demyelination, and other morphological alterations in axons of peripheral nerves. These changes may, in turn, induce changes in the generation and propagation of action potentials in peripheral nerves, leading to decreased transmission of information from peripheral sensory organs to the central nervous system.

Lipid oxidative damage and distribution of inorganic arsenic and its metabolites in the rat nervous system after arsenite exposure: influence of alpha tocopherol supplementation.

Inorganic arsenic (iAs) exposure causes peripheral neuropathy. Oxidative effects caused by iAs exposure in peripheral nerves have been incompletely characterized. This study analyzed arsenic and lipid oxidative damage in the brain, spinal cord, and sciatic and sensory sural nerves following arsenite exposure. This study also explored whether alpha tocopherol (alpha-TOC) administration mitigates arsenite-induced oxidative damage. Thiobarbituric acid-reactive substance (TBARS) levels and distributions of iAs and its metabolites were evaluated in male Wistar rats following 30d of sodium arsenite exposure (10mg/kg bodyweight (bw)/d, by gavage). A second group also received alpha-TOC (125mg/kg bw/d, by gavage) during the final 20d of arsenite administration. Arsenite exposure caused increased TBARS levels within each region of the nervous system; oxidative stress was most pronounced in the sural and sciatic nerves. In addition there was a positive quadratic relationship between TBARS levels and the concentration of arsenicals found in the nervous system (r(2)=0.878, p<0.001). Dimethylarsenic was the predominant metabolite of iAs found. Animals alpha-TOC-treated had a 1.7-5.2-fold reduction in TBARS levels when compared with rats that received iAs alone. These results suggest that oxidative damage may be the main mechanism of toxicity induced by exposure of the peripheral nervous system to arsenite and that such damage could be attenuated by alpha-TOC-supplementation.

Arsenite-induced formation of hydroxyl radical in the striatum of awake rats.

Recent studies on the mechanisms of arsenite toxicity report that some of its effects have been traced to the generation of reactive oxygen species during oxidative stress. In this study we analyze the formation of hydroxyl radicals in the brain of awake, freely moving rats, in order to obtain direct evidence of arsenic-induced oxidative stress in this tissue. We examined the time-course of hydroxyl radical formation in the striatum of both female and male rats who underwent a direct infusion during 60 min of different concentrations of arsenite in that structure through a microdialysis probe. We report here that basal levels of hydroxyl radical production in female rats are significantly higher than those in male rats (91.9+/-16.1 vs. 59.2+/-18.1 pmol/ml, P<0.001) and that the treatment with arsenite induced significant increases of hydroxyl radical formation over basal levels at 50, 100, 200 and 400 microM (95, 98, 98 and 99% increases, respectively, P<0.05 in all cases). The maximal response to 100 microM arsenite is significantly higher in female than in male rats (194.6+/-50.1 female rats and 88.1+/-11.6 pmol/ml male rats, P=0.036). These results support the participation of hydroxyl radicals in arsenic-induced disturbances in the central nervous system.