CAJ | 학술논문

目的探究叶酸能否在急性脑梗死的缺血再灌注中起到保护作用。方法 Sprague-Dawley大鼠，随机分为3组，对照组（n=8）、治疗组（n=12）和预处理组（n=16），均为常规饲料饲喂7 d。对照组和治疗组每日给予生理盐水；预处理组每日给予叶酸悬液。用腔内线栓法制作大脑中动脉闭塞（MCAO）模型，术后24 h拔出栓线，完成再灌注。手术日及术后，对照组注射生理盐水，预处理组和治疗组给予叶酸悬液。各组术后1~6 d内每日进行神经功能缺损评分，并于第6天行脑组织切片TTC染色，并分别取灌流区和梗死区组织用ELISA法测定单核细胞化学趋化因子-1（MCP-1）浓度。结果术后第6天评分，对照组、叶酸治疗组叶酸预防组分别为4.56±3.63、2.94±2.94和1.00±1.00。TTC染色对照组、叶酸治疗组叶酸预防组的梗死面积分别占全脑面积的44.23±10.06%、20.64±6.76%和14.61±13.51%。缺血区MCP-1浓度结果对照组、预防组和治疗组分别为(168.58±107.21)、152.91±64.78、97.74±46.19 ng/L。结论叶酸在急性脑梗死的缺血灌注中可能起到保护作用。
목적탐구협산능부재급성뇌경사적결혈재관주중기도보호작용。방법 Sprague-Dawley대서，수궤분위3조，대조조（n=8）、치료조（n=12）화예처리조（n=16），균위상규사료사위7 d。대조조화치료조매일급여생리염수；예처리조매일급여협산현액。용강내선전법제작대뇌중동맥폐새（MCAO）모형，술후24 h발출전선，완성재관주。수술일급술후，대조조주사생리염수，예처리조화치료조급여협산현액。각조술후1~6 d내매일진행신경공능결손평분，병우제6천행뇌조직절편TTC염색，병분별취관류구화경사구조직용ELISA법측정단핵세포화학추화인자-1（MCP-1）농도。결과술후제6천평분，대조조、협산치료조협산예방조분별위4.56±3.63、2.94±2.94화1.00±1.00。TTC염색대조조、협산치료조협산예방조적경사면적분별점전뇌면적적44.23±10.06%、20.64±6.76%화14.61±13.51%。결혈구MCP-1농도결과대조조、예방조화치료조분별위(168.58±107.21)、152.91±64.78、97.74±46.19 ng/L。결론협산재급성뇌경사적결혈관주중가능기도보호작용。
Objective To test whether folic acid offers protection of the brain tissue against acute cerebral infarction in rats. Methods Sprague-Dawley rats were divided into control (n=8), pre-treatment (n=12) and treatment (n=16) groups, all having routine feed for 7 days. The rats in the control and treatment groups were given normal saline daily, and those in the pre-treatment group received folic acid suspension daily. All the rats were then subject to middle cerebral artery occlusion (MCAO) for 24 h followed by reperfusion. On and after the operation day, the rats in the control group were given normal saline and those in the other two groups were given folic acid suspension daily. Neural function deficiency was evaluated on a daily basis after the operation, and on day 6 after the operation, brain biopsy was performed for examination with TTC staining. Monocyte chemokine-1 (MCP-1) in both normal and infarct tissues was measured by ELISA. Results On day 6 after the operation, the neural function deficiency scores of the control, pre-treatment and treatment groups were 4.56 ± 3.63, 2.94 ± 2.94 and 1.00 ± 1.00, and the percentages of the infarct area (to the whole brain area) were (44.23 ± 10.06)%, (20.64 ± 6.78)%and (14.61 ± 13.51)%, respectively. The contents of MCP-1 in the infarct area of the brain tissues were 168.58 ± 107.21 ng/L, 152.91 ± 64.78 ng/L, and 97.74 ± 46.19 ng/L in the 3 groups, respectively. Conclusion Folic acid can protect brain tissue against acute cerebral infarction in rats.