CAJ | 학술논문

目的：探讨缺血后处理对糖尿病大鼠脑组织一氧化氮（ NO）及一氧化氮合成酶（ NOS）含量的影响。方法将30只Wistar大鼠（180～200 g）按随机数字表法分为空白组、缺血组和缺血后处理组。均经一次性链脲佐菌素（STZ）腹腔注射建立糖尿病大鼠模型。缺血组和缺血后处理组大鼠结扎颈总动脉，造脑缺血模型，缺血后处理组对大鼠进行缺血后处理。 HE染色观察各组大鼠脑组织形态学变化，ELISA法检测大鼠血清中NO及NOS各亚型的含量变化，同时免疫印迹（ Western blot ）法检测脑组织中NOS蛋白的表达情况。结果缺血后处理组大鼠脑组织缺损降低，神经元细胞增多，与缺血组相比，缺血后处理组iNOS明显下降，差异具有统计学意义（ P ＜0.05），而与空白组大鼠差异无统计学意义（ P ＞0.05）。 WB结果显示，缺血后处理大鼠中iNOS的表达明显弱于缺血组（ P ＜0.05），与空白组差异无统计学意义（ P ＞0.05）。结论缺血后处理对糖尿病大鼠脑组织具有一定的保护作用，可能是通过抑制NOS特别是iNOS的活性，达到治疗的作用。
목적：탐토결혈후처리대당뇨병대서뇌조직일양화담（ NO）급일양화담합성매（ NOS）함량적영향。방법장30지Wistar대서（180～200 g）안수궤수자표법분위공백조、결혈조화결혈후처리조。균경일차성련뇨좌균소（STZ）복강주사건립당뇨병대서모형。결혈조화결혈후처리조대서결찰경총동맥，조뇌결혈모형，결혈후처리조대대서진행결혈후처리。 HE염색관찰각조대서뇌조직형태학변화，ELISA법검측대서혈청중NO급NOS각아형적함량변화，동시면역인적（ Western blot ）법검측뇌조직중NOS단백적표체정황。결과결혈후처리조대서뇌조직결손강저，신경원세포증다，여결혈조상비，결혈후처리조iNOS명현하강，차이구유통계학의의（ P ＜0.05），이여공백조대서차이무통계학의의（ P ＞0.05）。 WB결과현시，결혈후처리대서중iNOS적표체명현약우결혈조（ P ＜0.05），여공백조차이무통계학의의（ P ＞0.05）。결론결혈후처리대당뇨병대서뇌조직구유일정적보호작용，가능시통과억제NOS특별시iNOS적활성，체도치료적작용。
Objective To investigate effects of ischemic postconditioning on the nitric oxide ( NO) and nitric oxide synthase ( NOS) in diabetic rat brain tissues .Methods Thirty Wistar rats were diabetic models induced by intraperitoneal injuction of stepto-zotocin (STZ), and randomly divided into three groups: Control group (normal, diabetic), cerebral ischemia group, and ischemic postconditioning ( I-POST) group.The rats of cerebral ischemia group and ischemic postconditioning group were made model of cere -bral ischemia by ligation carotid artery .Hematoxylin-eosin ( HE) was used to observe their pathological changes in control and diabetic groups.Enzyme-linked immunosorbent assay ( ELISA) method was used to detect the expression and changes of NO and NOS in the sera in each group .Western Blot method was used to investigate the expression and changes of NOS in the retinal tissues in each group .Results For I-POST group , brain tissue defects were decreased , neuronal cells were increased , serum inducible NOS ( iNOS) content was significantly lower than endothelial NOS (eNOS) and neuronal NOS (nNOS) ( P <0.05), brain tissue iNOS expression was significantly weaker than ischemia group ( P <0.05 ) and was not different from normal group ( P >0.05 ) .Conclusions Is-chemic postconditioning can protect the brain tissue of diabetic rats by inhibiting NOS activity especially iNOS .