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N-acetylcysteine and glycyrrhizin combination:Benefit outcome in a murine model of acetaminophen-induced liver failure

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World Journal of Hepatology 2020年第9期12卷 596-618页

作者： Charlotte Minsart Sandrine Rorive Arnaud Lemmers Eric Quertinmont th.erry gustot Laboratory of Experimental Gastroenterology Erasme HospitalUniversitéLibre de BruxellesBrussels 1070Belgium Department of Pathology Erasme HospitalUniversitéLibre de BruxellesBrussels 1070Belgium DIAPAth-Center for Microscopy and Molecular Imaging UniversitéLibre de BruxellesGosselies 6041Belgium Department of Gastroenterology Hepato Pancreatology and Digestive OncologyErasme HospitalUniversitéLibre de BruxellesBrussels 1070Belgium Inserm Unité1149 Centre de Recherche sur l’inflammationParis 75006France UMR S_1149 UniversitéParis DiderotParis 75006France

BACKGROUND Acetaminophen overdose is the most frequent cause of drug-induced liver failure in developed *** progress has been made in understanding the mechanism of hepatocellular injury,but N-acetylcysteine remains the only effective treatment despite its short therapeutic ***,other hepatoprotective drugs are needed for the delayed treatment of acetaminopheninduced *** interest focused on glycyrrhizin for its role as an inhibitor of high mobility group box 1(HMGB1)protein,a member of the family of damage-associated molecular pattern,known to play an important pathological role in various *** To investigate the efficacy of the N-acetylcysteine/glycyrrhizin combination compared to N-acetylcysteine alone in the prevention of liver *** Eight-week-old C57BL/6J wild-type female mice were used for all our *** fasted for 15 h were treated with acetaminophen(500 mg/kg)or vehicle(phosphate-buffered saline)by intraperitoneal injection and separated into the following groups:Glycyrrhizin(200 mg/kg);N-acetylcysteine(150 mg/kg);and N-acetylcysteine/*** all groups,mice were sacrificed 12 h following acetaminophen *** assessment of hepatotoxicity was performed by measuring plasma levels of alanine aminotransferase,aspartate aminotransferase and lactate *** was also evaluated by histological examination of hematoxylin and eosin-stained tissues *** rates were compared between various groups using Kaplan-Meier *** Consistent with data published in the literature,we confirmed that intraperitoneal administration of acetaminophen(500 mg/kg)in mice induced severe liver injury as evidenced by increases in alanine aminotransferase,aspartate aminotransferase and lactate dehydrogenase but also by liver necrosis *** administration was shown to reduce the release of HMGB1 and significantly decreased the severity of liver injury.

关键词： Acetaminophen Acute liver injury Glycyrrhizin N-acetylcysteine Nacetylcysteine/glycyrrhizin combination Murine model High mobility group box 1

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克罗恩病的可溶性细胞因子受体类型

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世界核心医学期刊文摘（胃肠病学分册） 2005年第8期1卷 40-41页

作者： gustot T Lemmers A Louis E 赵天智 Division of Gastroenterol ogy Erasme University Hospital Free University of Brussels 808 Lennik St 107 0 Brussels Belgium.Dr

Introduction: Soluble cytokine receptors (sCRs) modulate the in vivo activity of cytokines. Deficient sCR production could participate in the pathogenesis and course of Crohn’s disease(CD). the aim of the study was to examine the pro- file of sCRs in CD patients and their modulation by infliximab and corticoster ***: We prospectively examined active CD patients(aCD) treated with eit her infliximab (n=21) or corticosteroids(n=9), CD patients in clinical remission (rCD, n=20), ulcerative colitis patients (UC, n=24), and healthy subjects (HS, n=15). Cultures of colonic biopsies were also examined from CD inflamed (n=8), C D non-inflamed (n=7), and healthy mucosa(n=8). Levels of tumour necrosis factor α(TNF-α), soluble TNF receptor I (sTNFRI), soluble TNF receptor II (sTNFRII) ,interleukin 1 β(IL-1 β), soluble IL-1 receptor I (sIL-1 RI),soluble IL-1 receptor II (sIL-1 RII), IL-6, soluble IL-6 receptor(sIL-6R), and sgp 130 we re measured using ELISA. Results:Higher levels of sTNFRI (Pth rCD and HS. Interestingl y, sIL-1 RII (Pth rCD and HS, and were negatively correlated with C RP. Deficient production of sIL-1 RII was specific to CD (not observed in ulcer ative colitis), and was further con-firmed at the mucosal level. Infliximab dec reased sTNFRII at one and four weeks (Pth dysregulated production of sCRs. Deficien cy in sIL-1 RII and sgp 130 may be essential to CD pathogenesis. their replacem ent through the use of fusion proteins could represent future alternative therap eutic strategies for CD.

关键词：克罗恩病溃疡性结肠炎临床缓解期皮质激素治疗单抗治疗活检标本细胞因子活体内肿瘤坏死因子α 白细胞介素

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