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Prophylaxis with ketotifen in rats with portal hypertension:involvement of mast cell and eicosanoids

Hepatobiliary & Pancreatic Diseases International 2008年第4期7卷 383-394页

作者： Fernando Sánchez-Patán Raquel Anchuelo elena vara Cruz García Yolanoa Saavedra Patri Vergara Carmen Cuellar Marta Rodero Maria-Angeles Aller Jaime Arias Department of Surgery I School of Medicine Complutense University of MadridSpain Department of Biochemistry and Molecular Biology School of Medicine Complutense University of MadridSpain Department of Physiology Autonoma University of BarcelonaSpain Department of Parasithology School of PharmacyComplutense University of MadridSpain

BACKGROUND:Since we have previously shown an increase of mast cells in the small bowel and in the mesenteric lymph nodes in the rats with prehepatic portal hypertension,it can be hypothesized that this essential inflammatory cell would be involved in the pathogeny of the splanchnic changes related to portal hypertension. METHODS:To verify this hypothesis,we first studied mast cell infiltration in the ileum and in the mesenteric lymph nodes in sham-operated male Wistar rats(n=12) and in short-term prehepatic portal hypertensive rats (n=12),and the serum levels of rat mast cell protease Ⅱ(RMCP-Ⅱ)by *** a second set of experiments ketotifen,a mast cell stabilizer drug,was administered to sham-operated(n=10)and portal hypertensive(n=12) rats 24 hours before the intervention and prostanoids (PGE2,PGI2,TXB2)and leukotrienes(LTC4,LTB4)were assayed by RIA,mast cell infiltration in the ileum and in the mesenteric lymph nodes and the serum levels of RMCP-Ⅱwere also studied,to show its effectiveness to prevent the mesenteric alterations produced by the inflammatory mediators released by the mast cell. RESULTS:Forty-eight hours after the intervention RMCP-Ⅱ (P<0.05),PGE2(P<0.001)and LTC4 serum levels decreased and mast cell number and RMCP-Ⅱlevels increased in mesenteric lymph nodes in portal hypertensive *** administration of ketotifen reduced portal pressure(P<0.001),serum levels of PGE2(P<0.001)and RMCP-Ⅱ(P<0.001)in mesenteric lymph nodes. CONCLUSIONS:In acute portal hypertension in the rat,the mast cell translocation from intestinal mucosa to mesenteric lymph nodes,where they are activated and degranulates,would represent a defence mechanism to avoid the activation of an acute and massive inflammatory response in this *** administration of ketotifen is able to reduce the splanchnic inflammatory changes related to acute portal hypertension in the rat.

关键词： portal hypertension prostaglandins leukotrienes mast cell

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Hepatic lipid metabolism changes in short-and long-term prehepatic portal hypertensive rats

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World Journal of Gastroenterology 2006年第42期12卷 6828-6834页

作者： Maria-Angeles Aller elena vara Cruz García Maria-Paz Nava Alejandra Angulo Fernando Sánchez-Patán Ana Calderón Patri Vergara Jaime Arias SurgeryⅠ Department School of Medicine Complutense University of Madrid Spain Biochemical and Molecular Biology Department School of Medicine Complutense University of Madrid Spain Animal Physiology Department (Physiology Ⅱ) School of Biological Sciences Complutense University of Madrid Spain Physiology Unit. Veterinary School Autonoma University of Barcelona Bellaterra Catalua Spain

AIM: To verify the impairment of the hepatic lipid metabolism in prehepatic portal hypertension. METHODS: The concentrations of free fatty acids, diacylglycerol, triglycerides, and phospholipids were assayed by using D-[U-14C] glucose incorporation in the different lipid fractions and thin-layer chromatography and cholesterol was measured by spectrophotometry, in liver samples of Wistar rats with partial portal vein ligation at short- (1 mo) and long-term (1 year) (i.e. portal hypertensive rats) and the control rats. RESULTS: In the portal hypertensive rats, liver phospholipid synthesis significantly decreased (7.42 ± 0.50 vs 4.70 ± 0.44 nCi/g protein; P < 0.01) and was associated with an increased synthesis of free fatty acids (2.08 ± 0.14 vs 3.36 ± 0.33 nCi/g protein; P < 0.05), diacylglycerol (1.93 ± 0.2 vs 2.26 ± 0.28 nCi/g protein), triglycerides (2.40 ± 0.30 vs 4.49 ± 0.15 nCi/g protein) and cholesterol (24.28 ± 2.12 vs 57.66 ± 3.26 mg/g protein; P < 0.01). CONCLUSION: Prehepatic portal hypertension in rats impairs the liver lipid metabolism. This impairment consists in an increase in lipid deposits (triglycerides,diacylglycerol and cholesterol) in the liver, accompanied by a decrease in phospholipid synthesis.

关键词： Portal hypertension Free fatty acids Diacylglycerides Triglycerides Phospholipids Cholesterol

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Endoscopic response to tumor necrosis factor inhibitors predicts long term benefits in Crohn's disease

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World Journal of Gastroenterology 2019年第14期25卷 1764-1774页

作者： Ignacio Alfaro Maria Carme Masamunt Nuria Planell Alicia López-García Jesús Castro Marta Gallego Rebeca Barastegui Angel Giner Alejandro vara Azucena Salas elena Ricart Julián Panés Ingrid Ordás Gastroenterology Department Hospital Clínic de Barcelona Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) University of Barcelona

BACKGROUND Identifying predictors of therapeutic response is the cornerstone of personalized *** To identify predictors of long-term mucosal healing(MH) in patients with Crohn's disease(CD) treated with tumor necrosis factor α(TNF-α) *** Prospective single center study. Consecutive patients with clinically active CD requiring treatment with a TNF-α inhibitor were included. A baseline segmental CD Endoscopic Index of Severity(CDEIS) ≥ 10 in at least one segment or the presence of ulcerations were required for inclusion. Clinical, biological and endoscopic data were obtained at baseline, weeks 14 and 46. Endoscopic response(ER) was defined as a decrease ≥ 50% from baseline CDEIS and MH as partial CDEIS ≤ 5 in all *** Of 62 patients were included. At baseline, median CD Activity Index and CDEIS were 201 and 6.7, respectively with a significant reduction after one year of treatment(53 and 3.0 respectively, P < 0.001). At week 14, 56% of patients achieved ER and 34% MH. At week 46, the corresponding percentages were 52%and 44%. Baseline disease characteristics or biomarkers did not predict MH. A decrease from baseline CDEIS at week 14 of at least 80% was the best predictor of MH at week 46(59% sensitivity and 91% specificity; area under the curve =0.778).CONCLUSION Clinical and biomarker data are not useful predictors of response to TNF-αinhibitors in CD, whereas ER to induction therapy, defined as 80% reduction in global CDEIS, is a robust predictor of long-term MH. Achievement of this endoscopic endpoint may be considered as a therapeutic target for anti-TNF-αtherapy.

关键词： Crohn’s disease Endoscopy Mucosal healing Crohn’s Disease Endoscopic Index of Severity Tumor necrosis factor

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