摘要
目的:探讨CD8+T细胞在早期内毒素血症心脏损伤中的浸润及其对心功能的影响。方法:野生雄性小鼠20只随机分为野生对照组和野生内毒素血症组,每组各10只;CD8敲除雄性小鼠10只,随机分为CD8敲除对照组和CD8敲除内毒素血症组,每组各5只。对照组均给予0.9%氯化钠液腹腔注射,内毒素血症组均给予脂多糖腹腔注射。6 h显微超声检测射血分数及短轴缩短分数;即刻处死并收取野生对照组及野生内毒素血症组各3只小鼠心脏组织,流式细胞技术检测心脏细胞悬液中巨噬细胞(F4/80+细胞)及CD8+T细胞、CD4+T细胞分布;其余小鼠心脏组织进行病理切片HE染色,观察心肌纤维断裂及炎症细胞浸润。结果:与野生对照组相比,野生内毒素血症组射血分数及短轴缩短分数显著降低(均为P<0.05);野生内毒素血症组F4/80+细胞、CD4+T细胞及CD8+T细胞均显著增加(均为P<0.05)。与野生内毒素血症组相比,CD8基因敲除内毒素血症组射血分数及短轴缩短分数均显著升高(均为P<0.05)。结论:急性内毒素血症导致心肌纤维损伤、心功能不全,心脏组织CD8+T等炎症细胞浸润;而缺乏CD8+T细胞时则减轻内毒素血症导致的心功能损伤,提示CD8+T细胞在急性内毒素血症诱导的心功能不全早期发挥重要作用。
Objective：To evaluate the involvement and effect of CD8^＋T cells in endotoxemia induced cardiac injury.Methods：Two groups of C57BL/6 wild-type mice were injected with saline（n=10） and LPS（n=10） separately;two groups of CD8 knockout mice were injected with saline and LPS separately.Cardiac function was evaluated by ultrasound 6 hr after LPS injection.Flow cytometry analysis was used to determine F4/80^＋,CD8^＋T cells,CD4^＋T cells infiltration in the heart of wild-type LPS injected or control group（n=3 for each group）.The rest mice were sacrificed and hearts were undergone HE staining analysis.Results：The ultrasound result showed that the LPS injection significantly deceased cardiac function（as evaluated by ejection fraction（EF%） and FS%,P〈0.05）,but CD8 knockout prevented LPS-induced cardiac dysfunction.HE staining showed LPS injection induced inflammatory cells infiltration and FACS analysis demonstrated that LPS injection stimulated F4/80^＋,CD4^＋T cells and CD8^＋T cells infiltration into the heart（P〈0.05）.Conclusion：Endotoxemia caused cardiac dysfunction by inducing the infiltration of inflammatory cells especially CD8^＋T cells into the heart,however,knockout of CD8 prevented endotoxemia-induced heart dysfunction.Our results indicated that CD8^＋T cells may play an important role in endotoxemia-induced heart failure,however the underlie mechanism need to be further investigated.
出处
《心肺血管病杂志》
CAS
2012年第2期200-203,共4页
Journal of Cardiovascular and Pulmonary Diseases
基金
国家自然科学基金(30888004)
国家自然科学基金(30971471)
