CAJ | 학술논문

目的评价富氢液对大鼠脑缺血再灌注时磷酸化p38丝裂原激活蛋白激酶(p-p38MAPK)表达的影响.方法健康雄性SD大鼠72只,体重220 ～ 250 g,采用随机数字表法分为3组(n=24):假手术组(S组)、脑缺血再灌注组(I/R组)和富氢液组(I/RH组).I/R组和I/RH组采用线栓法制备大鼠脑缺血再灌注损伤模型,缺血2h,再灌注24 h;I/RH组于术前3d及再灌注即刻腹腔注射富氢液(0.6 mmol/L) 10 ml/kg,S组和I/R组注射等容量生理盐水.于再灌注24 h时行神经功能缺陷评分,取脑组织,TTC法测定脑梗死体积,计算脑梗死体积百分比;干湿法测定脑含水量;采用TUNEL法检测大脑细胞凋亡情况,计算细胞凋亡指数;采用免疫组化法及Western blot法检测p38MAPK、和p-p38MAPK的表达.观察脑组织病理学结果.结果与S组比较,I/R组和I/RH组神经功能缺陷评分和细胞凋亡指数升高,脑含水量和脑梗死体积百分比增加,p38MAPK及p-p38MAPK表达上调(P＜0.05);与I/R组比较,I/RH组神经功能缺陷评分、细胞凋亡指数和脑含水量降低,脑梗死体积百分比减小,p38MAPK及p-p38MAPK表达下调(P＜0.05).I/RH组脑组织病理学损伤程度较I/R组减轻.结论富氢液通过抑制p-p38MAPK表达,减少细胞凋亡,从而减轻大鼠脑缺血再灌注损伤.
목적 평개부경액대대서뇌결혈재관주시린산화p38사렬원격활단백격매(p-p38MAPK)표체적영향.방법 건강웅성SD대서72지,체중220 ～ 250 g,채용수궤수자표법분위3조(n=24):가수술조(S조)、뇌결혈재관주조(I/R조)화부경액조(I/RH조).I/R조화I/RH조채용선전법제비대서뇌결혈재관주손상모형,결혈2h,재관주24 h;I/RH조우술전3d급재관주즉각복강주사부경액(0.6 mmol/L) 10 ml/kg,S조화I/R조주사등용량생리염수.우재관주24 h시행신경공능결함평분,취뇌조직,TTC법측정뇌경사체적,계산뇌경사체적백분비;간습법측정뇌함수량;채용TUNEL법검측대뇌세포조망정황,계산세포조망지수;채용면역조화법급Western blot법검측p38MAPK、화p-p38MAPK적표체.관찰뇌조직병이학결과.결과 여S조비교,I/R조화I/RH조신경공능결함평분화세포조망지수승고,뇌함수량화뇌경사체적백분비증가,p38MAPK급p-p38MAPK표체상조(P＜0.05);여I/R조비교,I/RH조신경공능결함평분、세포조망지수화뇌함수량강저,뇌경사체적백분비감소,p38MAPK급p-p38MAPK표체하조(P＜0.05).I/RH조뇌조직병이학손상정도교I/R조감경.결론 부경액통과억제p-p38MAPK표체,감소세포조망,종이감경대서뇌결혈재관주손상.
Objective To evaluate the effect of hydrogen-rich saline on the expression of phosphor-p38 mitogen-activated protein kinase (p-p38MAPK) during cerebral ischemia-reperfusion (I/R) in rats.Methods Seventy-two adult male Sprague-Dawley rats,weighing 220-250 g,were randomly divided into 3 groups (n =20 each) using a random number table:sham operation group (group S),I/R group and hydrogen-rich saline group (group I/RH).Cerebral ischemia was induced in chloral hydrate-anesthetized rats by 2 h middle cerebral artery occlusion in I/R and I/RH groups.The artery was only exposed but not occluded in group S.At 3 days before operation and immediately after onset of reperfusion,hydrogen-rich saline (0.6 mmol/L) 10 ml/kg was intraperitoneally injected in group I/RH,while the equal volume of normal saline was given in S and I/R groups.Neurological deficits were blindly assessed and scored at the end of 24 h reperfusion.The animals were then sacrificed,and brains were removed for microscopic examination and for determination of the cerebral infarct size (by TTC),brain water content,cell apoptosis (by TUNEL),and expression of p38MAPk and phosphor-p38MAPK (p-p38MAPK) (by immunohistochemistry and Western blot).Apoptosis index was calculated.Results Compared with group S,neurological deficit score,apoptosis index,brain water content and cerebral infarct size were significantly increased,and the expression of p38MAPK and p-p38MAPK was up-regulated in I/R and I/RH groups.Compared with group I/R,neurological deficit score,apoptosis index,brain water content and cerebral infarct size were significantly decreased,and the expression of p38MAPK and p-p38MAPK was down-regulated in group I/RH.The pathological changes of cerebral tissues were significantly attenuated in group I/RH as compared with group I/R.Conclusion Hydrogen-rich saline can reduce cell apoptosis through inhibiting p-p38MAPK expression,thus attenuating cerebral I/R injury in rats.