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Donghyun Kim - One of the best experts on this subject based on the ideXlab platform.
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Kakkalide and irisolidone alleviate 2,4,6-Trinitrobenzenesulfonic Acid-induced colitis in mice by inhibiting lipopolysaccharide binding to toll-like receptor-4 and proteobacteria population.
International immunopharmacology, 2019Co-Authors: Hyo-min Jang, Keon-tae Park, Hyun-deok Noh, So-hyeon Lee, Donghyun KimAbstract:The flower of Pueraria lobata (family Fabaceae) has been clinically used in traditional Chinese medicine to counteract symptoms associated with drinking alcohol and liver injury and to alleviate inflammatory diseases. Its major constituent kakkalide is metabolized to irisolidone by gut microbiota. This research study was undertaken to understand the anti-colitis mechanism of kakkalide and irisolidone in vitro and in vivo. Kakkalide and its metabolite irisolidone inhibited lipopolysaccharide (LPS)-stimulated NF-κB activation and TNF-α expression in macrophages. They also inhibited LPS-induced phosphorylation of IRAK1 and TAK1 and activation of NF-κB by inhibiting the binding of Alexa Fluor 488-conjugated LPS in vitro. Orally administered irisolidone or kakkalide alleviated colon shortening and myeloperoxidase activity in mice with 2,4,6-Trinitrobenzenesulfonic Acid (TNBS)-induced colitis. Their treatments also protected epithelial cell disruption and infiltration of CD11b+/CD11c+ cells in the colon. Furthermore, they suppressed TNBS-induced expression of M1 macrophage markers TNF-α, CD80, CD86, and Arg2 expression while the expression of M2 macrophage markers Arg1, CD163, CD206, and IL-10 was induced. They also suppressed the fecal Proteobacteria population. Overall, the anti-colitic effects of irisolidone were superior to those of kakkalide. Kakkalide and its metabolite irisolidone inhibited inflammation in vitro and in vivo by inhibiting LPS binding to toll-like receptor 4 and gut proteobacteria population.
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Ocotillol, a Majonoside R2 Metabolite, Ameliorates 2,4,6-Trinitrobenzenesulfonic Acid-Induced Colitis in Mice by Restoring the Balance of Th17/Treg Cells.
Journal of agricultural and food chemistry, 2015Co-Authors: Sang-yun Lee, Jin-ju Jeong, Thi Hong Van Le, Su-hyeon Eun, Minh D. Nguyen, Jeong Hill Park, Donghyun KimAbstract:In a preliminary experiment, majonoside R2 (MR2), isolated from Vietnamese ginseng (Panax vietnamensis Ha et Grushv.), inhibited differentiation to Th17 cells and was metabolized to ocotillol via pseudoginsenoside RT4 (PRT4) by gut microbiota. Therefore, we examined the inhibitory effects of MR2 and its metabolites PRT4 and ocotillol against Th17 cell differentiation. These ginsenosides significantly suppressed interleukin (IL)-6/tumor growth factor beta-induced differentiation of splenic CD4(+) T cells into Th17 cells and expression of IL-17 in vitro. Among these ginsenosides, ocotillol showed the highest inhibitory effect. We also examined the anti-inflammatory effect of ocotillol in mice with 2,4,6-Trinitrobenzenesulfonic Acid (TNBS)-induced colitis. Oral administration of ocotillol significantly suppressed TNBS-induced colon shortening, macroscopic score, myeloperoxidase activity, and production of nitric oxide and prostaglandin E2. Ocotillol treatment increased TNBS-suppressed expression of tight junction proteins ZO-1, occludin, and claudin-1 in the colon. Treatment with ocotillol inhibited TNBS-induced expression of tumor necrosis factor (TNF)-α and IL-1β, as well as activation of NF-κB and MAPKs. Moreover, treatment with ocotillol inhibited TNBS- induced differentiation to Th17 cells in the lamina propria of colon, as well as expression of T-bet, RORγt, IL-17, and IL-23. Ocotillol treatment also increased Treg cell differentiation and Foxp3 and IL-10 expression. These findings suggest that orally administered MR2 may be metabolized to ocotillol in the intestine by gut microbiota and the transformed ocotillol may ameliorate inflammatory diseases such as colitis by restoring the balance of Th17/Treg cells.
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ocotillol a majonoside r2 metabolite ameliorates 2 4 6 Trinitrobenzenesulfonic Acid induced colitis in mice by restoring the balance of th17 treg cells
Journal of Agricultural and Food Chemistry, 2015Co-Authors: Sang-yun Lee, Jin-ju Jeong, Thi Hong Van Le, Su-hyeon Eun, Minh D. Nguyen, Jeong Hill Park, Donghyun KimAbstract:In a preliminary experiment, majonoside R2 (MR2), isolated from Vietnamese ginseng (Panax vietnamensis Ha et Grushv.), inhibited differentiation to Th17 cells and was metabolized to ocotillol via pseudoginsenoside RT4 (PRT4) by gut microbiota. Therefore, we examined the inhibitory effects of MR2 and its metabolites PRT4 and ocotillol against Th17 cell differentiation. These ginsenosides significantly suppressed interleukin (IL)-6/tumor growth factor beta-induced differentiation of splenic CD4(+) T cells into Th17 cells and expression of IL-17 in vitro. Among these ginsenosides, ocotillol showed the highest inhibitory effect. We also examined the anti-inflammatory effect of ocotillol in mice with 2,4,6-Trinitrobenzenesulfonic Acid (TNBS)-induced colitis. Oral administration of ocotillol significantly suppressed TNBS-induced colon shortening, macroscopic score, myeloperoxidase activity, and production of nitric oxide and prostaglandin E2. Ocotillol treatment increased TNBS-suppressed expression of tight junction proteins ZO-1, occludin, and claudin-1 in the colon. Treatment with ocotillol inhibited TNBS-induced expression of tumor necrosis factor (TNF)-α and IL-1β, as well as activation of NF-κB and MAPKs. Moreover, treatment with ocotillol inhibited TNBS- induced differentiation to Th17 cells in the lamina propria of colon, as well as expression of T-bet, RORγt, IL-17, and IL-23. Ocotillol treatment also increased Treg cell differentiation and Foxp3 and IL-10 expression. These findings suggest that orally administered MR2 may be metabolized to ocotillol in the intestine by gut microbiota and the transformed ocotillol may ameliorate inflammatory diseases such as colitis by restoring the balance of Th17/Treg cells.
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Glycosaminoglycan degradation-inhibitory lactic Acid bacteria ameliorate 2,4,6-Trinitrobenzenesulfonic Acid-induced colitis in mice.
Journal of microbiology and biotechnology, 2009Co-Authors: Bomi Lee, Junghee Lee, Hye-sung Lee, Eun-ah Bae, Chul-sung Huh, Young-tae Ahn, Donghyun KimAbstract:To evaluate the effects of lactic Acid bacteria (LAB) in inflammatory bowel diseases (IBD), we measured the inhibitory effect of several LAB isolated from intestinal microflora and commercial probiotics against the glycosaminoglycan (GAG) degradation by intestinal bacteria. Bifidobacterium longum HY8004 and Lactobacillus plantarum AK8-4 exhibited the most potent inhibition. These LAB inhibited colon shortening and myeloperoxidase production in 2,4,6- Trinitrobenzenesulfonic Acid (TNBS)-induced experimental colitic mice. These LAB also blocked the expression of the proinflammatory cytokines, IL-1beta and TNF-alpha, as well as of COX-2, in the colon. LAB also blocked activation of the transcription factor, NF-kappaB, and expression of TLR-4 induced by TNBS. In addition, LAB reduced the TNBS-induced bacterial degradation activities of chondroitin sulfate and hyaluronic Acid. These findings suggest that GAG degradation-inhibitory LAB may improve colitis by inhibiting inflammatory cytokine expression via TLR-4-linked NF-kB activation and by inhibiting intestinal bacterial GAG degradation.
Antonio Zarzuelo - One of the best experts on this subject based on the ideXlab platform.
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Intestinal anti-inflammatory activity of apigenin K in two rat colitis models induced by Trinitrobenzenesulfonic Acid and dextran sulphate sodium.
The British journal of nutrition, 2015Co-Authors: Cristina Mascaraque, Antonio Zarzuelo, María Dolores Suárez, Raquel González, Fermín Sánchez De Medina, Olga Martínez-augustinAbstract:Flavonoids are polyphenolic compounds that are widespread in nature, and consumed as part of the human diet in significant amounts. The aim of the present study was to test the intestinal anti-inflammatory activity of apigenin K, a soluble form of apigenin, in two models of rat colitis, namely the Trinitrobenzenesulfonic Acid (TNBS) model and the dextran sulphate sodium (DSS) model. Apigenin K (1, 3 and 10 mg/kg; by the oral route; n 4-6 per group) was administered as a pre-treatment to rats with TNBS and DSS colitis, and colonic status was checked by macroscopic and biochemical examination. Apigenin K pre-treatment resulted in the amelioration of morphological signs and biochemical markers in the TNBS model. The results demonstrated a reduction in the inflamed area, as well as lower values of score and colonic weight:length ratio compared with the TNBS group. Myeloperoxidase (MPO) activity was reduced by 30 % (P< 0·05). Moreover, apigenin K pre-treatment ameliorated morphological signs and biochemical markers in the DSS model. Thus, macroscopic damage was significantly reduced and the colonic weight:length ratio was lowered by approximately 10 %, while colonic MPO and alkaline phosphatase activities were decreased by 35 and 21 %, respectively (P< 0·05). Apigenin K pre-treatment also tended to normalise the expression of a number of colonic inflammatory markers (e.g. TNF-α, transforming growth factor-β, IL-6, intercellular adhesion molecule 1 or chemokine (C-C motif) ligand 2). In conclusion, apigenin K is found to have anti-inflammatory effects in two preclinical models of inflammatory bowel disease.
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Effect of kale and papaya supplementation in colitis induced by Trinitrobenzenesulfonic Acid in the rat
E-spen The European E-journal of Clinical Nutrition and Metabolism, 2010Co-Authors: Cibele Lima De Albuquerque, Anderson Luiz-ferreira, Alba Regina Monteiro De Souza Brito, Maria Elena Rodriguez-cabezas, Desiree Camuesco, Monica Comalada, Antonio Zarzuelo, Ana Nieto, Julio GalvezAbstract:Summary Background & aims Papaya and kale are usual vegetables in the Brazilian diet that have antioxidant activity. This study proposed to evaluate the effect of dried vegetables as a prebiotic and as an intestinal anti-inflammatory in the rat colitis model. Methods Rats received, orally, 500 mg/kg of rat weight of three treatments of dried vegetables: papaya, kale and the mixture of both vegetables (60% of kale plus 40% of papaya). In the prebiotic study, after two weeks of treatment, bacteria counts were determined. In the anti-inflammatory study, after the two weeks of treatment, colitis was induced by intracolonic administration of Trinitrobenzenesulfonic Acid (TNBS), and one week after, damage score and biochemical parameters were evaluated. Results Only the administration of the mixture was able to modulate the bacterial flora in healthy rats, as well as in rats with colitis induced by TNBS. In addition, the mixture showed intestinal antiinflammatory effect in the colitic rats. This effect was evidenced by a reduction in damage score, by the colonic iNOS expression downregulated, by the decrease in the production of the TNFα and IL-1β and by the decrease in the MPO activity. Conclusion The combination of both vegetables showed prebiotic and anti-inflammatory effects in the TNBS model of rat colitis, when compared to each single vegetable alone.
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di d fructose dianhydride enriched caramels effect on colon microbiota inflammation and tissue damage in Trinitrobenzenesulfonic Acid induced colitic rats
Journal of Agricultural and Food Chemistry, 2010Co-Authors: B Arribas, Elena Suarezpereira, Carmen Ortiz Mellet, Jose Garcia M Fernandez, Christoph Buttersack, Maria Elena Rodriguezcabezas, Natividad Garridomesa, Elvira Bailon, Eduardo Guerrahernandez, Antonio ZarzueloAbstract:In the present study we describe the preparation and chemical characterization of a caramel with a high (70%) content of difructose dianhydrides (DFAs) and glycosylated derivatives (DFAs). This product was obtained by thermal activation (90 °C) of highly concentrated (90% w/v) aqueous d-fructose solutions using the sulfonic Acid ion-exchange resin Lewatit S2328 as caramelization catalyst. DFAs represent a unique family of cyclic fructans with prebiotic properties already present in low proportions (<15%) in commercial caramel. We report the antiinflammatory activity of the new DFA-enriched caramel in the Trinitrobenzenesulfonic Acid (TNBS) model of rat colitis, an experimental model that resembles human inflammatory bowel disease (IBD), and compare its effects with those obtained with a commercial sucrose caramel and with linear fructooligosaccharides (FOS). For this purpose, the effects on colon tissue damage, gut microbiota, short-chain fatty Acid (SCFAs) production, and different inflammatory markers w...
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The bisphosphonate alendronate improves the damage associated with Trinitrobenzenesulfonic Acid-induced colitis in rats.
British journal of pharmacology, 2007Co-Authors: Isabel Ballester, Antonio Zarzuelo, Ana Nieto, Abdelali Daddaoua, Rocío López-posadas, María Dolores Suárez, Olga Martínez-augustin, F. Sánchez De MedinaAbstract:Background and purpose: The nitrogen-containing bisphosphonates are drugs used successfully in the treatment of osteoporosis. They act inhibiting farnesyl diphosphate synthase. This mechanism may also produce anti-inflammatory effects. The therapeutic activity of alendronate was tested in vivo using a model of inflammatory bowel disease. Experimental approach: The Trinitrobenzenesulfonic Acid model of colitis in the rat was used. Rats were treated orally with alendronate and its efficacy compared with that of oral sulphasalazine or vehicle, starting 2 h after colitis induction. The status of the animals was assessed 5 days later. Key results: Alendronate treatment (25 or 75 mg kg-1 day-1) resulted in a decrease in the colonic damage score and loss of body weight (at 25 mg kg-1 day-1 only). This was associated to a dramatic reduction in the mRNA levels of interleukin 1β (IL-1β), monocyte chemoattractant protein 1 (MCP-1) and interleukin 1 receptor antagonist (IL-1ra). The magnitude of the beneficial effect was comparable to that of sulphasalazine (at a 6-20 fold higher dose). Thus sulphasalazine post-treatment reduced the mRNA levels of IL-1β/IL-1ra and MCP-1 to the same extent as alendronate and additionally lowered colonic alkaline phosphatase activity, but failed to affect body weight loss or colonic damage score. Alendronate failed to exert beneficial effects when administered intraperitoneally. Conclusions and Implications: Oral but not intraperitoneal alendronate significantly protected the colon in experimental rat colitis. Inflammatory bowel disease patients might benefit from exposure to oral alendronate. British Journal of Pharmacology (2007) 151, 206–215. doi:10.1038/sj.bjp.0707227
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A comparative study of the preventative effects exerted by two probiotics, Lactobacillus reuteri and Lactobacillus fermentum , in the Trinitrobenzenesulfonic Acid model of rat colitis
The British journal of nutrition, 2007Co-Authors: Laura Peran, Monica Comalada, Antonio Zarzuelo, Ana Nieto, Elvira Bailon, Saleta Sierra, Federico Lara-villoslada, Ángel Concha, Mónica Olivares, Jordi XausAbstract:The intestinal anti-inflammatory effects of two probiotics isolated from breast milk, Lactobacillus reuteri and L. fermentum, were evaluated and compared in the Trinitrobenzenesulfonic Acid (TNBS) model of rat colitis. Colitis was induced in rats by intracolonic administration of 10 mg TNBS dissolved in 50% ethanol (0.25 ml). Either L. reuteri or L. fermentum was daily administered orally (5 x 10(8) colony-forming units suspended in 0.5 ml skimmed milk) to each group of rats (n 10) for 3 weeks, starting 2 weeks before colitis induction. Colonic damage was evaluated histologically and biochemically, and the colonic luminal contents were used for bacterial studies and for SCFA production. Both probiotics showed intestinal anti-inflammatory effects in this model of experimental colitis, as evidenced histologically and by a significant reduction of colonic myeloperoxidase activity (P
Sang-yun Lee - One of the best experts on this subject based on the ideXlab platform.
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Ocotillol, a Majonoside R2 Metabolite, Ameliorates 2,4,6-Trinitrobenzenesulfonic Acid-Induced Colitis in Mice by Restoring the Balance of Th17/Treg Cells.
Journal of agricultural and food chemistry, 2015Co-Authors: Sang-yun Lee, Jin-ju Jeong, Thi Hong Van Le, Su-hyeon Eun, Minh D. Nguyen, Jeong Hill Park, Donghyun KimAbstract:In a preliminary experiment, majonoside R2 (MR2), isolated from Vietnamese ginseng (Panax vietnamensis Ha et Grushv.), inhibited differentiation to Th17 cells and was metabolized to ocotillol via pseudoginsenoside RT4 (PRT4) by gut microbiota. Therefore, we examined the inhibitory effects of MR2 and its metabolites PRT4 and ocotillol against Th17 cell differentiation. These ginsenosides significantly suppressed interleukin (IL)-6/tumor growth factor beta-induced differentiation of splenic CD4(+) T cells into Th17 cells and expression of IL-17 in vitro. Among these ginsenosides, ocotillol showed the highest inhibitory effect. We also examined the anti-inflammatory effect of ocotillol in mice with 2,4,6-Trinitrobenzenesulfonic Acid (TNBS)-induced colitis. Oral administration of ocotillol significantly suppressed TNBS-induced colon shortening, macroscopic score, myeloperoxidase activity, and production of nitric oxide and prostaglandin E2. Ocotillol treatment increased TNBS-suppressed expression of tight junction proteins ZO-1, occludin, and claudin-1 in the colon. Treatment with ocotillol inhibited TNBS-induced expression of tumor necrosis factor (TNF)-α and IL-1β, as well as activation of NF-κB and MAPKs. Moreover, treatment with ocotillol inhibited TNBS- induced differentiation to Th17 cells in the lamina propria of colon, as well as expression of T-bet, RORγt, IL-17, and IL-23. Ocotillol treatment also increased Treg cell differentiation and Foxp3 and IL-10 expression. These findings suggest that orally administered MR2 may be metabolized to ocotillol in the intestine by gut microbiota and the transformed ocotillol may ameliorate inflammatory diseases such as colitis by restoring the balance of Th17/Treg cells.
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ocotillol a majonoside r2 metabolite ameliorates 2 4 6 Trinitrobenzenesulfonic Acid induced colitis in mice by restoring the balance of th17 treg cells
Journal of Agricultural and Food Chemistry, 2015Co-Authors: Sang-yun Lee, Jin-ju Jeong, Thi Hong Van Le, Su-hyeon Eun, Minh D. Nguyen, Jeong Hill Park, Donghyun KimAbstract:In a preliminary experiment, majonoside R2 (MR2), isolated from Vietnamese ginseng (Panax vietnamensis Ha et Grushv.), inhibited differentiation to Th17 cells and was metabolized to ocotillol via pseudoginsenoside RT4 (PRT4) by gut microbiota. Therefore, we examined the inhibitory effects of MR2 and its metabolites PRT4 and ocotillol against Th17 cell differentiation. These ginsenosides significantly suppressed interleukin (IL)-6/tumor growth factor beta-induced differentiation of splenic CD4(+) T cells into Th17 cells and expression of IL-17 in vitro. Among these ginsenosides, ocotillol showed the highest inhibitory effect. We also examined the anti-inflammatory effect of ocotillol in mice with 2,4,6-Trinitrobenzenesulfonic Acid (TNBS)-induced colitis. Oral administration of ocotillol significantly suppressed TNBS-induced colon shortening, macroscopic score, myeloperoxidase activity, and production of nitric oxide and prostaglandin E2. Ocotillol treatment increased TNBS-suppressed expression of tight junction proteins ZO-1, occludin, and claudin-1 in the colon. Treatment with ocotillol inhibited TNBS-induced expression of tumor necrosis factor (TNF)-α and IL-1β, as well as activation of NF-κB and MAPKs. Moreover, treatment with ocotillol inhibited TNBS- induced differentiation to Th17 cells in the lamina propria of colon, as well as expression of T-bet, RORγt, IL-17, and IL-23. Ocotillol treatment also increased Treg cell differentiation and Foxp3 and IL-10 expression. These findings suggest that orally administered MR2 may be metabolized to ocotillol in the intestine by gut microbiota and the transformed ocotillol may ameliorate inflammatory diseases such as colitis by restoring the balance of Th17/Treg cells.
Michael A. Pezzone - One of the best experts on this subject based on the ideXlab platform.
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enhanced expression of mast cell growth factor and mast cell activation in the bladder following the resolution of Trinitrobenzenesulfonic Acid tnbs colitis in female rats
Neurourology and Urodynamics, 2007Co-Authors: Ruomei Liang, Elena E. Ustinova, Radhika Patnam, Matthew O. Fraser, Dmitriy W. Gutkin, Michael A. PezzoneAbstract:Aims Chronic pelvic pain disorders often overlap. We have shown that acute colonic irritation can produce acute irritative micturition patterns and acutely sensitize bladder afferent responses to mechanical and chemical stimuli. We hypothesize that with time, colonic irritation can lead to neurogenic changes in the bladder and the development of chronic bladder sensitization. Methods Micturition patterns were measured in rats 60–90 days after the induction of Trinitrobenzenesulfonic Acid (TNBS) colitis in the resolution phase of this model. Total and activated mast cells (MCs) were quantified in the bladder, while mRNA levels of stem cell factor (SCF; a.k.a. MC growth factor) and nerve growth factor (NGF; a MC and nociceptive C-fiber stimulator) were quantified in the bladder and L6-S1 dorsal root ganglia (DRG). Results Following intra-rectal TNBS, voiding volume was reduced (P < 0.005), while voiding frequency was increased (P < 0.05), both by ∼50%. Furthermore, both the percentage and density of activated bladder MCs were significantly elevated (P < 0.05), although total MC counts were not statistically increased. At the molecular level, urinary bladder SCF expression increased twofold (P < 0.005), as did NGF (P < 0.01), while L6-S1 DRG levels were not significantly elevated. Conclusions Chronic cystitis in the rat as evidenced by changes in micturition patterns and the recruitment of activated MCs can occur during the resolution phase of TNBS colitis. These changes, of which MCs may play an important role, appear to be maintained over time and may occur via stimulation of convergent pelvic afferent input resulting in the upregulation of neurotrophic factors in the target organ. Neurourol. Urodynam. 26:887–893, 2007. © 2007 Wiley-Liss, Inc.
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Enhanced expression of mast cell growth factor and mast cell activation in the bladder following the resolution of Trinitrobenzenesulfonic Acid (TNBS) colitis in female rats
Neurourology and urodynamics, 2007Co-Authors: Ruomei Liang, Elena E. Ustinova, Radhika Patnam, Matthew O. Fraser, Dmitriy W. Gutkin, Michael A. PezzoneAbstract:Aims Chronic pelvic pain disorders often overlap. We have shown that acute colonic irritation can produce acute irritative micturition patterns and acutely sensitize bladder afferent responses to mechanical and chemical stimuli. We hypothesize that with time, colonic irritation can lead to neurogenic changes in the bladder and the development of chronic bladder sensitization. Methods Micturition patterns were measured in rats 60–90 days after the induction of Trinitrobenzenesulfonic Acid (TNBS) colitis in the resolution phase of this model. Total and activated mast cells (MCs) were quantified in the bladder, while mRNA levels of stem cell factor (SCF; a.k.a. MC growth factor) and nerve growth factor (NGF; a MC and nociceptive C-fiber stimulator) were quantified in the bladder and L6-S1 dorsal root ganglia (DRG). Results Following intra-rectal TNBS, voiding volume was reduced (P
Gabriele Brecchia - One of the best experts on this subject based on the ideXlab platform.
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Probiotic mixture supplementation in the preventive management of Trinitrobenzenesulfonic Acid-induced inflammation in a murine model
Journal of biological regulators and homeostatic agents, 2016Co-Authors: Giovanna Traina, Laura Menchetti, Francesca Rappa, Patrizia Casagrande-proietti, Olimpia Barbato, Lucio Leonardi, Francesco Carini, Federica Piro, Gabriele BrecchiaAbstract:Inflammatory bowel diseases (IBD) are characterized by inflammatory conditions of the intestine. Probiotic bacteria (PB) can have beneficial effects in several gastrointestinal disorders. The objectives of this study were: (i) to provide an acute experimental IBD model induced by 2,4,6-Trinitrobenzenesulfonic Acid (TNBS) in CD-1 mice, and (ii) to assess the preventive effects of Citogenex (Lactobacillus casei and Bifidobacterum lactis) supplementation on intestinal tissues and microbiota. Mice were inoculated intrarectally with saline, ethanol or different TNBS solutions. 1%TNBS induced clinical signs of colitis (P less than 0.01) and histological damage (P less than 0.01). Based on these results, mice were pre-treated with Citogenex or saline for 1, 2 or 3 weeks before 1%TNBS treatment. Probiotic pre-treatment determined a reduction of clinical signs (P less than 0.05), histological alterations of colitis (P less than 0.05) and increased beneficial bacteria (P less than 0.05). This study confirms that TNBS-induced colitis in CD-1 mice is useful for studying the mechanisms involved in IBD pathogenesis, and pre-treatment with Citogenex prevents the intestinal damage induced by TNBS.
