Effects of non-caloric ultrashort wave on the expression of CoQ10 and C1GALT1C1 in rats with cerebral ischemia reperfusion injury

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.
[Article in English, Chinese]

Abstract

Objectives: To examine the changes of coenzyme Q10 (CoQ10) and β1,3-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.

Methods: Fifty SD rats were randomly divided into 5 groups (n=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.

Results: 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 P<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 P<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 P<0.05).

Conclusions: 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.

目的: 探讨脑缺血再灌注损伤大鼠在不同时间点予以无热量超短波(ultrashort wave,USW)治疗后脑内辅酶Q10(coenzyme Q10,CoQ10)、β1,3-半乳糖基转移酶-特异性伴侣1(β1,3-galactosyl transferase specific chaperone 1,C1GALT1C1)表达水平的变化趋势及其对缺血性脑损伤的保护机制。方法: 50只Sprague-Dawley大鼠随机分为5组,每组10只。1组是作为对照的假手术组,线栓插入深度为1 cm;其余4组为实验组(分别为模型1 d组、USW1 d组、模型3 d组、USW3 d组),线栓插入深度为18 mm,2 h后予以再灌注。4个实验组中,每组随机选取5只大鼠行盐酸2,3,5-三苯基四氮(2,3,5-triphenyltetrazoliumchloride,TTC)染色,其余5只大鼠行蛋白质印迹法和real-time PCR检测,观察比较各组大鼠脑梗死体积百分比值和缺血侧大脑中CoQ10和C1GALT1C1的相对表达量。结果: TTC染色后所得脑梗死体积百分比值中,假手术组未见脑梗死,比值为0;实验组随着病程延长和USW治疗呈下降趋势,差异均有统计学意义(均P<0.05)。蛋白质印迹法和real-time PCR检测显示:假手术组CoQ10相对表达量最高,但实验组CoQ10相对表达量随着病程延长和USW治疗呈上升趋势,差异均有统计学意义(均P<0.05);假手术组C1GALT1C1的相对表达量最低,但实验组C1GALT1C1的相对表达量随着病程延长和USW治疗呈下降趋势,差异均有统计学意义(均P<0.05)。结论: 无热量USW治疗脑缺血再灌注损伤大鼠,可能通过上调CoQ10表达及下调C1GALT1C1表达而发挥保护作用。.

Keywords: cerebral ischemia reperfusion injury; coenzyme Q10; ultrashort wave; β 1,3-galactosyl transferase specific chaperone 1.

MeSH terms

  • Animals
  • Brain
  • Brain Ischemia*
  • Molecular Chaperones
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury*
  • Ubiquinone / analogs & derivatives

Substances

  • Molecular Chaperones
  • Ubiquinone
  • coenzyme Q10