Chen Rao, Peng Longkai, Yan Yihong, Fan Yongmei
Department of Rehabilitation, Second Xiangya Hospital, Central South University, Changsha 410011, China.
Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2020 Jan 28;45(1):24-34. doi: 10.11817/j.issn.1672-7347.2020.180523.
To examine the changes of coenzyme Q10 (CoQ10) and β-galactosyl transferase specific chaperone 1 (C1GALT1C1) in brain of rats with ischemic injury at different time points and to explore the protective mechanism of ultrashort wave (USW) on ischemic brain injury.
Fifty SD rats were randomly divided into 5 groups (=10 per group): a sham group (control group) and 4 experimental group (ischemia for 2 h). The 4 experimental groups were set as a model 1 d group, a USW 1 d group, a model 3 d group and a USW 3 d group, respectively. Five rats were randomly selected for 2,3,5-triphenyltetrazoliumchloride (TTC) staining in each experimental group, and the remaining 5 rats were subjected to Western blotting and real-time PCR. The percentage of cerebral infarction volume and the relative expression level of CoQ10 and C1GALT1C1 in the brain were examined and compared.
The infarct volume percentage after TTC staining was zero in the sham group. With the progress of disease and USW therapy, the infarct volume percentage was decreased in the experimental groups (all <0.05); Western blotting and real-time PCR showed that the relative expression level of CoQ10 in the sham group was the highest, while in the experimental groups, the content of CoQ10 showed a upward trend with the extension of disease and USW therapy, with significant difference (all <0.05). The relative expression level of C1GALT1C1 in the sham group was the lowest, but in the experimental groups, they showed a downward trend with the extension of disease and USW therapy, with significant difference (all <0.05).
Non-caloric USW therapy may upregulate the expression of CoQ10 to suppress the expression of C1GALT1C1 in rats, leading to alleviating cerebral ischemic reperfusion injury.
观察缺血性损伤大鼠不同时间点脑内辅酶Q10（CoQ10）和β-半乳糖基转移酶特异性伴侣蛋白1（C1GALT1C1）的变化，探讨超短波（USW）对缺血性脑损伤的保护机制。
将50只SD大鼠随机分为5组（每组n = 10）：假手术组（对照组）和4个实验组（缺血2 h）。4个实验组分别设为模型1 d组、超短波1 d组、模型3 d组和超短波3 d组。每组随机选取5只大鼠进行2,3,5-三苯基氯化四氮唑（TTC）染色，其余5只大鼠进行蛋白质免疫印迹法（Western blotting）和实时荧光定量聚合酶链反应（real-time PCR）。检测并比较脑梗死体积百分比以及脑内CoQ10和C1GALT1C1的相对表达水平。
假手术组TTC染色后梗死体积百分比为零。随着病情进展和超短波治疗，各实验组梗死体积百分比均降低（均P < 0.05）；蛋白质免疫印迹法和实时荧光定量聚合酶链反应结果显示，假手术组CoQ10相对表达水平最高，各实验组CoQ10含量随病情进展和超短波治疗呈上升趋势，差异有统计学意义（均P < 0.05）。假手术组C1GALT1C1相对表达水平最低，各实验组C1GALT1C1相对表达水平随病情进展和超短波治疗呈下降趋势，差异有统计学意义（均P < 0.05）。
非热量超短波治疗可能上调大鼠CoQ10表达，抑制C1GALT1C1表达，从而减轻脑缺血再灌注损伤。
