严重高甘油三酯血症小鼠血液流变学的异常分析

Analysis of the Hemorheological Abnormalities in Mice with Severe Hypertriglyceridemia

目的:本研究旨在检测两种严重高甘油三酯血症(HTG)小鼠的血液流变学,建立具有异常血液流变学特点的HTG小鼠模型,以应用于进一步的相关机制研究。方法:采用ApoC3转基因与GPIHBP1基因敲除的HTG小鼠及野生型小鼠,所用小鼠均为C57BL/6J背景下8周龄雄性小鼠,通过生物物理法检测和比较其血浆粘度、红细胞渗透脆性、变形性与电泳率。结果:与野生小鼠相比,ApoC3转基因与GPIHBP1基因敲除的HTG小鼠血浆甘油三酯含量明显升高(P<0.05),红细胞渗透脆性显著增加(P<0.05),变形指数与电泳率明显降低(P<0.05),血浆粘度显著升高(P<0.05),但血细胞计数等血常规指标均未见显著差异(P>0.05)。结论:Apo C3tg与GPIHBP1KO小鼠血液流变学发生异常改变,可能作为探讨HTG血液流变学异常和动脉粥样硬化心血管疾病病理机制的动物模型。

Objective: To establish a mouse model of hypertriglyceridemia with hemorheological abnormalities for mechanisms researches. Methods: ApoC3 gene transgenic and GPIHBP1 gene knock-out mice with severe hypertriglyceridemia were used to detect the plasma viscosity, erythrocyte osmotic fragility, deformity, and electrophoresis rate by biophysical methods in comparison with the wild type mice. All C57BL/6J male mice were aged 8 weeks. Results: Compared with the wild-type group, severe hypertriglyceridemic mice had higher plasma levels of triglyceride, increased plasma viscosity, larger osmotic fragility, lower maximum erythrocyte deformation index, lower erythrocyte electrophoresis rate of red blood cells(P<0.05). However, no significant change was observed in the blood cell counts between two groups. Conclusions: ApoC3 transgenic and GPIHBP1 knock-out mice demonstrated hemorheological abnormalities. These two mouse models might be applied for the researches on pathological mechanisms for atherosclerotic cardiovascular disease with between hemorheological abnormalities under severe hypertriglyceridemia.