Lei Hong, Xu Jian, Cheng Li-Juan, Guo Qi, Deng An-Mei, Li Yong-Shen
Institute for Drug and Instrument Control of Beijing Military Area Command, , Beijing, China.
Department of Laboratory Medicine, Chang Hai Hospital, Second Military Medical University, Shanghai, China.
Clinics (Sao Paulo). 2014 Jun;69(6):426-32. doi: 10.6061/clinics/2014(06)10.
Our study aimed to investigate the impact of fatigue on the severity of stroke and to explore the underlying mechanisms.
Fatigued male rats underwent middle cerebral artery occlusion and the infarcted brain area was determined. Then, coagulation parameters were assessed in the fatigued group and a control group. In addition, the level of fibrinogen was determined in rats deprived of sleep for various numbers of days. To study whether interleukin-6 was involved in fibrinogen synthesis during fatigue, we also measured levels of interleukin-6 in rats deprived of sleep for various numbers of days. Furthermore, brain injury by middle cerebral artery occlusion was measured in wild-type mice, interleukin-6-/- mice and wild-type mice treated with bezafibrate.
More severe cerebral infarction was observed in the fatigued rats, resulting in an infarct ratio of 23.4%. The infarct ratio was significantly increased in the fatigued rats compared with that in the control group (8%, p<0.05). The level of fibrinogen was increased significantly in the fatigued rats compared with that in the control group. In addition, a marked reduction in fibrinogen level was observed in the fatigued interleukin-6-/- mice compared to their wild-type counterparts, whereas no difference was observed between fatigued wild-type mice and interleukin-6-/- rats treated with recombinant human interleukin-6. The reduction in brain injury due to middle cerebral artery occlusion during fatigue was observed in interleukin-6-/- mice and wild-type mice treated with bezafibrate.
Fatigue could increase stroke severity and was associated with the interleukin-6-induced expression of fibrinogen.
本研究旨在探讨疲劳对中风严重程度的影响，并探索其潜在机制。
对疲劳的雄性大鼠进行大脑中动脉闭塞手术，并测定梗死脑区面积。然后，评估疲劳组和对照组的凝血参数。此外，测定不同天数睡眠剥夺大鼠的纤维蛋白原水平。为研究白细胞介素-6是否参与疲劳期间纤维蛋白原的合成，我们还测定了不同天数睡眠剥夺大鼠的白细胞介素-6水平。此外，在野生型小鼠、白细胞介素-6基因敲除小鼠以及用苯扎贝特治疗的野生型小鼠中，测量大脑中动脉闭塞所致的脑损伤。
在疲劳大鼠中观察到更严重的脑梗死，梗死率为23.4%。与对照组（8%）相比，疲劳大鼠的梗死率显著增加（p<0.05）。与对照组相比，疲劳大鼠的纤维蛋白原水平显著升高。此外，与野生型对应小鼠相比，疲劳的白细胞介素-6基因敲除小鼠的纤维蛋白原水平显著降低，而疲劳的野生型小鼠与用重组人白细胞介素-6治疗的白细胞介素-6基因敲除大鼠之间未观察到差异。在白细胞介素-6基因敲除小鼠和用苯扎贝特治疗的野生型小鼠中，观察到疲劳期间大脑中动脉闭塞所致脑损伤的减轻。
疲劳可增加中风严重程度，并与白细胞介素-6诱导的纤维蛋白原表达有关。
