中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2013年
33期
5981-5987
,共7页
张振强%宋军营%贾亚泉%李澎涛%潘彦舒
張振彊%宋軍營%賈亞泉%李澎濤%潘彥舒
장진강%송군영%가아천%리팽도%반언서
组织构建%组织构建实验造模%高脂血症%单纯脑缺血%基础性病变%脑组织%病理学分析%脑缺血%TTC染色%苏木精-伊红染色%部级基金
組織構建%組織構建實驗造模%高脂血癥%單純腦缺血%基礎性病變%腦組織%病理學分析%腦缺血%TTC染色%囌木精-伊紅染色%部級基金
조직구건%조직구건실험조모%고지혈증%단순뇌결혈%기출성병변%뇌조직%병이학분석%뇌결혈%TTC염색%소목정-이홍염색%부급기금
背景:大多数脑缺血是在高血压、高脂血症、糖尿病等基础病变条件下发生的。因此,构建高脂血症复合脑缺血大鼠模型,研究基础性病变对脑缺血的影响具有重要意义。<br> 目的:观察高脂血症复合脑缺血大鼠模型脑组织病理学改变,及其高脂血症病理因素对脑缺血的影响。<br> 方法:实验以高脂饲料喂养大鼠制备高脂血症大鼠模型,然后线栓法制备局灶性脑缺血大鼠模型,建模成功后3,7 d,采用TTC染色的方法,观察各组大鼠脑组织缺血部位体积,苏木精-伊红染色观察各组大鼠脑组织缺血边缘区组织病理学改变,透射电镜观察各组大鼠脑组织缺血边缘区细胞超微结构改变。<br> 结果与结论:TTC染色结果显示高脂+脑缺血7 d组大鼠的脑缺血部位体积明显减小。苏木精-伊红染色结果显示所有脑缺血模型都呈典型的缺血性改变,脑缺血7d的小胶质细胞数量比3d的明显减少,高脂+脑缺血7d相对于3 d的变化更明显。超微结构显示所有脑缺血模型的神经元和胶质细胞核膜皱缩,线粒体嵴基本完全消失,内皮细胞线粒体减少,神经突触的突触小泡大部分溶解,缺血7 d,尤其是高脂+脑缺血7 d的上述损伤减轻,神经元变性、坏死减少,线粒体损伤恢复,线粒体嵴也明显增多,神经突触的突触小泡明显恢复。说明高脂血症促进了脑缺血损伤的恢复,其原因可能是高脂血症因素激活了体内某种保护机制。
揹景:大多數腦缺血是在高血壓、高脂血癥、糖尿病等基礎病變條件下髮生的。因此,構建高脂血癥複閤腦缺血大鼠模型,研究基礎性病變對腦缺血的影響具有重要意義。<br> 目的:觀察高脂血癥複閤腦缺血大鼠模型腦組織病理學改變,及其高脂血癥病理因素對腦缺血的影響。<br> 方法:實驗以高脂飼料餵養大鼠製備高脂血癥大鼠模型,然後線栓法製備跼竈性腦缺血大鼠模型,建模成功後3,7 d,採用TTC染色的方法,觀察各組大鼠腦組織缺血部位體積,囌木精-伊紅染色觀察各組大鼠腦組織缺血邊緣區組織病理學改變,透射電鏡觀察各組大鼠腦組織缺血邊緣區細胞超微結構改變。<br> 結果與結論:TTC染色結果顯示高脂+腦缺血7 d組大鼠的腦缺血部位體積明顯減小。囌木精-伊紅染色結果顯示所有腦缺血模型都呈典型的缺血性改變,腦缺血7d的小膠質細胞數量比3d的明顯減少,高脂+腦缺血7d相對于3 d的變化更明顯。超微結構顯示所有腦缺血模型的神經元和膠質細胞覈膜皺縮,線粒體嵴基本完全消失,內皮細胞線粒體減少,神經突觸的突觸小泡大部分溶解,缺血7 d,尤其是高脂+腦缺血7 d的上述損傷減輕,神經元變性、壞死減少,線粒體損傷恢複,線粒體嵴也明顯增多,神經突觸的突觸小泡明顯恢複。說明高脂血癥促進瞭腦缺血損傷的恢複,其原因可能是高脂血癥因素激活瞭體內某種保護機製。
배경:대다수뇌결혈시재고혈압、고지혈증、당뇨병등기출병변조건하발생적。인차,구건고지혈증복합뇌결혈대서모형,연구기출성병변대뇌결혈적영향구유중요의의。<br> 목적:관찰고지혈증복합뇌결혈대서모형뇌조직병이학개변,급기고지혈증병리인소대뇌결혈적영향。<br> 방법:실험이고지사료위양대서제비고지혈증대서모형,연후선전법제비국조성뇌결혈대서모형,건모성공후3,7 d,채용TTC염색적방법,관찰각조대서뇌조직결혈부위체적,소목정-이홍염색관찰각조대서뇌조직결혈변연구조직병이학개변,투사전경관찰각조대서뇌조직결혈변연구세포초미결구개변。<br> 결과여결론:TTC염색결과현시고지+뇌결혈7 d조대서적뇌결혈부위체적명현감소。소목정-이홍염색결과현시소유뇌결혈모형도정전형적결혈성개변,뇌결혈7d적소효질세포수량비3d적명현감소,고지+뇌결혈7d상대우3 d적변화경명현。초미결구현시소유뇌결혈모형적신경원화효질세포핵막추축,선립체척기본완전소실,내피세포선립체감소,신경돌촉적돌촉소포대부분용해,결혈7 d,우기시고지+뇌결혈7 d적상술손상감경,신경원변성、배사감소,선립체손상회복,선립체척야명현증다,신경돌촉적돌촉소포명현회복。설명고지혈증촉진료뇌결혈손상적회복,기원인가능시고지혈증인소격활료체내모충보호궤제。
BACKGROUND:Cerebral ischemia often occurs in underlying pathological conditions, such as hypertension, <br> hyperlipidemia and diabetes. Therefore, it is of great significance to construct a cerebral ischemia rat model with hyperlipidemia and to study the effect of basic pathological changes on the cerebral ischemia. <br> OBJECTIVE:To observe the brain tissue pathological changes of rat models with coexistence of hyperlipidemia and cerebral ischemia, and the effect of hyperlipidmia on cerebral ischemia. <br> METHODS:The rats were fed with high-fat diet to establish the hyperlipidmia models, and then focal cerebral <br> ischemia models were prepared with suture method. At 3 and 7 days after modeling, the 2,3,5-triphenyltetrazolium chloride staining was used to observe the volume of brain tissue ischemia, and hematoxylin-eosin staining was <br> performed to observe pathological change of the margin of the brain tissue ischemia zone. <br> RESULTS AND CONCLUSION:2,3,5-Triphenyltetrazolium chloride staining staining results showed that the volume of cerebral ischemia was significantly reduced in the hyperlipidemia+cerebral ischemia 7 day group. Hematoxylin-eosin staining results showed there was typical ischemic changes in al the cerebral ischemia models, and the number of microglial cel s after cerebral ischemia for 7 days was significantly smal er than that after cerebral ischemia for 3 days, and the changes were more obvious in the hyperlipidemia+7-day cerebral ischemia group when compared with the hyperlipidemia+3-day cerebral ischemia group. Ultrastructure showed there were neuronal and glial nuclear membrane shrinkage in al the cerebral ischemia models, mitochondria cristae was disappeared completely, endothelial cel mitochondria was decreased, most of the synaptic vesicles of nerve synapse were dissolved;the damages above were improved after ischemia for 7 days, especial y <br> hyperlipidemia+cerebral ischemia for 7 days, the neuronal degeneration and necrosis were reduced, the <br> mitochondrial damage was repaired, the number of mitochondrial cristae was increased significantly, and the synaptic vesicles of nerve synapse were recovered significantly. The results indicate that hyperlipidemia can promote the recovery of cerebral ischemic injury, <br> probably because the hyperlipidemia factors can activate the protection mechanism.