肝脏缺血再灌注损伤引起的全身性炎症对瘦或肥胖内脏脂肪组织的影响

Ligia Fernanda Ferraz, C. R. P. Caria, R. D. C. Santos, M. Ribeiro, A. Gambero
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摘要

摘要目的:探讨肝缺血再灌注对瘦型和肥胖型小鼠肝脏损伤的影响。方法:瘦小鼠和饮食性肥胖小鼠肝脏缺血30 min,再灌注6 h。用细胞术分析内脏脂肪组织的血管间质部分,用Array法和RT-qPCR法检测基因表达。通过口服异硫氰酸荧光素-葡聚糖来评估肠通透性,通过鲎试剂溶出法测定血清内毒素来评估内毒素血症。结果:发现肝脏缺血再灌注后,瘦小鼠内脏脂肪组织中中性粒细胞、单核细胞、淋巴细胞浸润,编码细胞因子、趋化因子及其受体的基因表达增加。这种炎症反应与瘦小鼠内毒素血症的存在有关。然而,在肥胖小鼠的内脏脂肪组织中没有观察到这些变化。结论:肝脏缺血再灌注可引起瘦小鼠脂肪组织的急性炎症反应,其特征为强烈的趋化因子诱导和白细胞浸润;然而,炎症改变在肥胖脂肪组织中已经存在,肝脏缺血和再灌注不会进一步损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of systemic inflammation due to hepatic ischemia-reperfusion injury upon lean or obese visceral adipose tissue
ABSTRACT Purpose: To evaluate how the induction of liver damage by ischemia and reperfusion affects the adipose tissue of lean and obese mice. Methods: Lean and diet-induced obese mice were subjected to liver ischemia (30 min) followed by 6 h of reperfusion. The vascular stromal fraction of visceral adipose tissue was analyzed by cytometry, and gene expression was evaluated by an Array assay and by RT-qPCR. Intestinal permeability was assessed by oral administration of fluorescein isothiocyanate (FITC)-dextran and endotoxemia by serum endotoxin measurements using a limulus amebocyte lysate assay. Results: It was found that, after liver ischemia and reperfusion, there is an infiltration of neutrophils, monocytes, and lymphocytes, as well as an increase in the gene expression that encode cytokines, chemokines and their receptors in the visceral adipose tissue of lean mice. This inflammatory response was associated with the presence of endotoxemia in lean mice. However, these changes were not observed in the visceral adipose tissue of obese mice. Conclusions: Liver ischemia and reperfusion induce an acute inflammatory response in adipose tissue of lean mice characterized by an intense chemokine induction and leukocyte infiltration; however, inflammatory alterations are already present at baseline in the obese adipose tissue and liver ischemia and reperfusion do not injure further.
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