首页> 美国卫生研究院文献>Mediators of Inflammation >Pretreatment with Fish Oil-Based Lipid Emulsion Modulates Muscle Leukocyte Chemotaxis in Murine Model of Sublethal Lower Limb Ischemia
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Pretreatment with Fish Oil-Based Lipid Emulsion Modulates Muscle Leukocyte Chemotaxis in Murine Model of Sublethal Lower Limb Ischemia

机译:鱼油基脂质乳剂预处理可调节亚致死性下肢缺血小鼠模型中的肌肉白细胞趋化性。

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摘要

This study investigated the effects of a fish oil- (FO-) based lipid emulsion on muscle leukocyte chemotaxis and inflammatory responses in a murine model of limb ischemia-reperfusion (IR) injury. Mice were assigned randomly to 1 sham (sham) group, 2 ischemic groups, and 2 IR groups. The sham group did not undergo the ischemic procedure. The mice assigned to the ischemic or IR groups were pretreated intraperitoneally with either saline or FO-based lipid emulsion for 3 consecutive days. The IR procedure was induced by applying a 4.5 oz orthodontic rubber band to the left thigh above the greater trochanter for 120 min and then cutting the band to allow reperfusion. The ischemic groups were sacrificed immediately while the IR groups were sacrificed 24 h after reperfusion. Blood, IR-injured gastrocnemius, and lung tissues were collected for analysis. The results showed that FO pretreatment suppressed the local and systemic expression of several IR-induced proinflammatory mediators. Also, the FO-pretreated group had lower blood Ly6ChiCCR2hi monocyte percentage and muscle M1/M2 ratio than the saline group at 24 h after reperfusion. These findings suggest that FO pretreatment may have a protective role in limb IR injury by modulating the expression of proinflammatory mediators and regulating the polarization of macrophage.
机译:这项研究调查了鱼油(FO-)基脂质乳剂对肢体缺血再灌注(IR)小鼠模型中肌肉白细胞趋化性和炎症反应的影响。将小鼠随机分为1个假(假)组,2个缺血组和2个IR组。假手术组未进行缺血手术。连续3天,将分配给缺血或IR组的小鼠腹腔内用生理盐水或基于FO的脂质乳剂进行预处理。通过在大转子上方的左大腿上施加4.5oz的正畸橡皮筋120分钟,诱导IR程序,然后切开橡皮筋以进行再灌注。缺血组立即处死,而IR组在再灌注后24h处死。收集血液,红外线损伤的腓肠肌和肺组织进行分析。结果表明,FO预处理抑制了几种IR诱导的促炎介质的局部和全身表达。此外,FO预处理组在再灌注后24h时的血液中Ly6C s CCR2 hi 单核细胞百分数和肌肉M1 / M2比更低。这些发现表明,FO预处理可能通过调节促炎性介质的表达并调节巨噬细胞的极化而在肢体IR损伤中起保护作用。

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