时珍国医国药
時珍國醫國藥
시진국의국약
LISHIZHEN MEDICINE AND MATERIA MEDICA RESEARCH
2010年
3期
527-529
,共3页
吴岚%周素娴%刘开祥%俸军林
吳嵐%週素嫻%劉開祥%俸軍林
오람%주소한%류개상%봉군림
缺血再灌注%单核细胞趋化蛋白-1%肿瘤坏死因子-α%青藤碱
缺血再灌註%單覈細胞趨化蛋白-1%腫瘤壞死因子-α%青籐堿
결혈재관주%단핵세포추화단백-1%종류배사인자-α%청등감
Ischemia-reperfusion%MCP-1%TNF-α%Sinomenine
目的 探讨青藤碱( sinomenine ,Sin)对糖尿病大鼠脑缺血再灌注损伤单核细胞趋化蛋白-1(MCP-1)和肿瘤坏死因子-α(TNF-α)含量的影响.方法 采用高脂高糖饮食加腹腔注射小剂量链脲霉素建立糖尿病大鼠模型,造模成功后将大鼠随机分为假手术组、缺血再灌注组、Sin低剂量治疗组和Sin高剂量治疗组.线栓法建立局灶性脑缺血再灌注模型.Sin低(30 mg/kg)、高剂量(60 mg/kg)治疗组于术前30 min分别给予大鼠腹腔注射.采用酶联免疫吸附实验( ELISA)法检测缺血90 min再灌注24 h大鼠额顶部皮质MCP-1和TNF-α含量的变化,并进行2,3,5-三苯基氯化四氮唑(TTC)染色和HE染色观察脑梗塞体积及病理形态学变化.结果 ①脑缺血再灌注24h,缺血再灌注组MCP-1和TNF-α含量明显升高,与假手术组比较,差异具有显著性(均P<0.05);与缺血再灌注组比较,Sin高、低剂量治疗组均显著减少MCP-1和TNF-α含量;高、低剂量组之间差异亦具有显著性(P<0.05);②Sin治疗组脑梗塞体积较缺血再灌注组减小,高、低剂量组之间差异亦具有显著性(P<0.05);③Sin高、低剂量治疗组脑组织缺血损伤病理学改变明显轻于缺血再灌注组,Sin高剂量治疗组缺血改变亦轻于低剂量治疗组.结论 Sin对糖尿病大鼠缺血再灌注脑损伤具有保护作用,其机制可能与降低缺血再灌注损伤脑组织MCP-1和TNF-α含量,抑制再灌注损伤炎症反应有关.
目的 探討青籐堿( sinomenine ,Sin)對糖尿病大鼠腦缺血再灌註損傷單覈細胞趨化蛋白-1(MCP-1)和腫瘤壞死因子-α(TNF-α)含量的影響.方法 採用高脂高糖飲食加腹腔註射小劑量鏈脲黴素建立糖尿病大鼠模型,造模成功後將大鼠隨機分為假手術組、缺血再灌註組、Sin低劑量治療組和Sin高劑量治療組.線栓法建立跼竈性腦缺血再灌註模型.Sin低(30 mg/kg)、高劑量(60 mg/kg)治療組于術前30 min分彆給予大鼠腹腔註射.採用酶聯免疫吸附實驗( ELISA)法檢測缺血90 min再灌註24 h大鼠額頂部皮質MCP-1和TNF-α含量的變化,併進行2,3,5-三苯基氯化四氮唑(TTC)染色和HE染色觀察腦梗塞體積及病理形態學變化.結果 ①腦缺血再灌註24h,缺血再灌註組MCP-1和TNF-α含量明顯升高,與假手術組比較,差異具有顯著性(均P<0.05);與缺血再灌註組比較,Sin高、低劑量治療組均顯著減少MCP-1和TNF-α含量;高、低劑量組之間差異亦具有顯著性(P<0.05);②Sin治療組腦梗塞體積較缺血再灌註組減小,高、低劑量組之間差異亦具有顯著性(P<0.05);③Sin高、低劑量治療組腦組織缺血損傷病理學改變明顯輕于缺血再灌註組,Sin高劑量治療組缺血改變亦輕于低劑量治療組.結論 Sin對糖尿病大鼠缺血再灌註腦損傷具有保護作用,其機製可能與降低缺血再灌註損傷腦組織MCP-1和TNF-α含量,抑製再灌註損傷炎癥反應有關.
목적 탐토청등감( sinomenine ,Sin)대당뇨병대서뇌결혈재관주손상단핵세포추화단백-1(MCP-1)화종류배사인자-α(TNF-α)함량적영향.방법 채용고지고당음식가복강주사소제량련뇨매소건립당뇨병대서모형,조모성공후장대서수궤분위가수술조、결혈재관주조、Sin저제량치료조화Sin고제량치료조.선전법건립국조성뇌결혈재관주모형.Sin저(30 mg/kg)、고제량(60 mg/kg)치료조우술전30 min분별급여대서복강주사.채용매련면역흡부실험( ELISA)법검측결혈90 min재관주24 h대서액정부피질MCP-1화TNF-α함량적변화,병진행2,3,5-삼분기록화사담서(TTC)염색화HE염색관찰뇌경새체적급병리형태학변화.결과 ①뇌결혈재관주24h,결혈재관주조MCP-1화TNF-α함량명현승고,여가수술조비교,차이구유현저성(균P<0.05);여결혈재관주조비교,Sin고、저제량치료조균현저감소MCP-1화TNF-α함량;고、저제량조지간차이역구유현저성(P<0.05);②Sin치료조뇌경새체적교결혈재관주조감소,고、저제량조지간차이역구유현저성(P<0.05);③Sin고、저제량치료조뇌조직결혈손상병이학개변명현경우결혈재관주조,Sin고제량치료조결혈개변역경우저제량치료조.결론 Sin대당뇨병대서결혈재관주뇌손상구유보호작용,기궤제가능여강저결혈재관주손상뇌조직MCP-1화TNF-α함량,억제재관주손상염증반응유관.
Objective To study the effect of sinomenine(Sin) on the contents of MCP-1 and TNF-αafter cerebral ischemia reperfusion(I/R) injury in diabetic rats.Methods In this experiment, rat model of diabetes mellitus was made by high sucrose , fat diet and streptozotion injection.Diabetic rats were randomly divided into 4 groups, namely sham operated group, I/R group,low dose Sin treated group and high dose Sin treated group. The focal middle cerebral artery occlusion(MCAO) model was made by suture-occluded method. Sin were given intraperitoneally to rats 30min before focal cerebral ischemia operation. After 90min MCAO following 24h of reperfusion,we investigated the contents of MCP-1 and TNF-α in ischemic frontal and parietal cortex . HE staining and TTC staining were also investigated. Results ①Compared with sham operated group , the contents of MCP-1 and TNF-α were increased at 24h of reperfusion in the ischemic territory(P<0.05). Compared with I/R group, Sin dose-dependently reduced the contents of MCP-1 and TNF-α (all P<0.05).②Compared with I/R group,cerebral infarction volume in low and highdose Sin treated groups was decreased dose-dependently (all P<0.05). ③The change of ischemic impairment in low or high dose Sin treated group was lighter than that of I/R group,and high dose Sin treated group was lighter than that of low dose Sin treated group.Conclusion Sin may reduced cerebral ischemia-reperfusion injury by decreasing the contents of MCP-1 and TNF-α in diabetic rats.