脂多糖处理诱导门脉高压大鼠胃粘膜适应性细胞保护

Malba E. A. Tavares, J. L. Barros, T. E. V. Lemos, Gerson J. N. Ferraz, J. M. Zeitune, J. Ferraz, Paula R. S. Camara
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摘要

目的:肝硬化和门静脉高压症患者的上消化道出血是一种常见的并发症,可能会影响这些患者的生存。这种现象的发生可能是由于过度的内毒素易位,导致系统调试肝脏过载,以及全身内毒素血症,免疫细胞过量产生介质。这些炎症介质的存在可能增加胃黏膜对各种损伤剂引起的病变的易感性。因此,本研究旨在确定门脉高压胃黏膜对内毒素和乙醇刺激的抵抗。方法:采用胆管结扎法或门静脉狭窄法诱导大鼠门脉高压,对照组假手术。通过急性或慢性LPS治疗,观察内毒素对胃黏膜的影响。通过离体胃室实验评估乙醇诱导的损伤。采用激光多普勒血流仪测量胃血流。结果:急性LPS处理(0.3 ~ 3 mg/kg)对健康(对照组)小鼠乙醇性胃损伤呈剂量依赖性增强。相比之下,PVS组胃黏膜在单剂量LPS (3mg /kg)后出现耐受。慢性LPS治疗(1 mg/kg)显著减少了PVS组和对照组胃粘膜病变面积。此外,肝硬化动物被发现不能在最低剂量的LPS下存活。结论:慢性LPS处理可诱导PVS大鼠和健康大鼠胃粘膜对乙醇损伤产生适应性细胞保护;然而,急性LPS治疗会增加肝硬化大鼠的死亡率。
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Lipopolysaccharide treatment induces adaptive cytoprotection in the portal hypertensive gastric mucosa of rats
Objective: Upper gastrointestinal bleeding in patients with cirrhosis and portal hypertension is a frequent complication that potentially modifies the survival of these patients. This phenomenon may occur due to excessive endotoxin translocation, leading to system debugging liver overload, and systemic endotoxemia, with excessive production of mediators by immune cells. The presence of these inflammatory mediators may increase the susceptibility of gastric mucosa to lesions induced by various damaging agents. As such, this study aimed to determine the resistance of portal hypertensive gastric mucosa to endotoxin and ethanol stimulation. Methods: Portal hypertension was induced in rats by bile duct ligation or portal vein stenosis (PVS) while controls underwent a sham operation. The effect of endotoxin on the gastric mucosa was evaluated by acute or chronic LPS treatment. Ethanol-induced damage was assessed using ex vivo gastric chamber experiments. Gastric blood flow was measured by laser Doppler flowmetry. Results: Acute LPS treatment intensified the ethanol-induced gastric damage in the healthy (control) group in a dose-dependent manner (0.3-3 mg/kg). In contrast, the gastric mucosa of the PVS group presented tolerance after a single dose of LPS (3 mg/kg). Chronic LPS treatment (1 mg/kg) significantly reduced the gastric mucosal lesion area in both the PVS and control groups. Additionally, the cirrhotic animals were found not to survive the minimum dose of LPS. Conclusion: Our results suggest that chronic LPS treatment induces adaptative cytoprotection to ethanol-induced injury in the gastric mucosa of PVS and healthy rats; however, acute LPS treatment increases mortality in cirrhotic rats.
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