中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
CHINESE JOURNAL OF EMERGENCY MEDICINE
2012年
6期
626-630
,共5页
张美齐%翟昌林%涂建锋%杨向红
張美齊%翟昌林%塗建鋒%楊嚮紅
장미제%적창림%도건봉%양향홍
丹参酮ⅡA%缺血-再灌注损伤%大鼠%高迁移率族蛋白1%表达
丹參酮ⅡA%缺血-再灌註損傷%大鼠%高遷移率族蛋白1%錶達
단삼동ⅡA%결혈-재관주손상%대서%고천이솔족단백1%표체
Tanshinone Ⅱ A%Ischemia-reperfusion injury%Rats%High mobility group box 1%Expression
目的 探讨丹参酮ⅡA(tanshinone,TSN)对大鼠脑缺血-再灌注损伤的保护作用及对高迁移率族蛋白1(high mobility group box 1,HMGBI)表达的影响.方法 雄性SD大鼠32只随机(随机数字法)分为4组(n=8),分别为假手术组(Sham组)、缺血-再灌注组(I/R组)、丹参酮ⅡA低剂量组(TaLD组)与丹参酮ⅡA高剂量组(TaHD组).采用右侧大脑中动脉栓塞(MCA0)法建立大鼠脑缺血-再灌注损伤模型.TTC染色法检测大鼠脑梗死体积,Tunnel法检测大脑皮质区细胞凋亡并计算凋亡指数,免疫印迹法检测大脑HMGB1的表达,ELISA法检测大鼠血清HMGB1水平,并测定大脑皮质钙调蛋白(calmodulin,CaM)活性及丙二醛(malondiadehyde,MDA)含量的变化.结果 与Sham组比较,I/R组、TaLD组与TaHD组大鼠脑梗死体积增大,凋亡细胞增多,CaM活性显著增强,MDA含量升高,脑组织及血清HMGBI水平明显升高(P＜0.01).与I/R组比较,TaLD、TaHD组脑梗死体积缩小、凋亡细胞减少,CaM活性显著减弱,MDA含量降低,脑组织及血清HMGB1水平明显降低(P＜0.01),且TaLD组与TaHD组之间上述各指标值差异具有统计学意义(P＜0.01).结论 丹参酮ⅡA能够减轻大鼠脑缺血-再灌注损伤,其机制可能与减轻脑缺血-再灌注阶段HMGB1介导的晚期炎症反应有关.
目的 探討丹參酮ⅡA(tanshinone,TSN)對大鼠腦缺血-再灌註損傷的保護作用及對高遷移率族蛋白1(high mobility group box 1,HMGBI)錶達的影響.方法 雄性SD大鼠32隻隨機(隨機數字法)分為4組(n=8),分彆為假手術組(Sham組)、缺血-再灌註組(I/R組)、丹參酮ⅡA低劑量組(TaLD組)與丹參酮ⅡA高劑量組(TaHD組).採用右側大腦中動脈栓塞(MCA0)法建立大鼠腦缺血-再灌註損傷模型.TTC染色法檢測大鼠腦梗死體積,Tunnel法檢測大腦皮質區細胞凋亡併計算凋亡指數,免疫印跡法檢測大腦HMGB1的錶達,ELISA法檢測大鼠血清HMGB1水平,併測定大腦皮質鈣調蛋白(calmodulin,CaM)活性及丙二醛(malondiadehyde,MDA)含量的變化.結果 與Sham組比較,I/R組、TaLD組與TaHD組大鼠腦梗死體積增大,凋亡細胞增多,CaM活性顯著增彊,MDA含量升高,腦組織及血清HMGBI水平明顯升高(P＜0.01).與I/R組比較,TaLD、TaHD組腦梗死體積縮小、凋亡細胞減少,CaM活性顯著減弱,MDA含量降低,腦組織及血清HMGB1水平明顯降低(P＜0.01),且TaLD組與TaHD組之間上述各指標值差異具有統計學意義(P＜0.01).結論 丹參酮ⅡA能夠減輕大鼠腦缺血-再灌註損傷,其機製可能與減輕腦缺血-再灌註階段HMGB1介導的晚期炎癥反應有關.
목적 탐토단삼동ⅡA(tanshinone,TSN)대대서뇌결혈-재관주손상적보호작용급대고천이솔족단백1(high mobility group box 1,HMGBI)표체적영향.방법 웅성SD대서32지수궤(수궤수자법)분위4조(n=8),분별위가수술조(Sham조)、결혈-재관주조(I/R조)、단삼동ⅡA저제량조(TaLD조)여단삼동ⅡA고제량조(TaHD조).채용우측대뇌중동맥전새(MCA0)법건립대서뇌결혈-재관주손상모형.TTC염색법검측대서뇌경사체적,Tunnel법검측대뇌피질구세포조망병계산조망지수,면역인적법검측대뇌HMGB1적표체,ELISA법검측대서혈청HMGB1수평,병측정대뇌피질개조단백(calmodulin,CaM)활성급병이철(malondiadehyde,MDA)함량적변화.결과 여Sham조비교,I/R조、TaLD조여TaHD조대서뇌경사체적증대,조망세포증다,CaM활성현저증강,MDA함량승고,뇌조직급혈청HMGBI수평명현승고(P＜0.01).여I/R조비교,TaLD、TaHD조뇌경사체적축소、조망세포감소,CaM활성현저감약,MDA함량강저,뇌조직급혈청HMGB1수평명현강저(P＜0.01),차TaLD조여TaHD조지간상술각지표치차이구유통계학의의(P＜0.01).결론 단삼동ⅡA능구감경대서뇌결혈-재관주손상,기궤제가능여감경뇌결혈-재관주계단HMGB1개도적만기염증반응유관.
Objective To investigate the influence of Tanshinone Ⅱ A on the expression of HMGB1 in rats with cerebral ischemia-reperfusion (I/R) injury and its neural function protection.Methods The 32 male SD rats were randomly (random number) divided into 4 groups (8 rats per group):Sham group,I/R group,group with low dose of Tanshinone Ⅱ A ( TaLD group) and group with high dose of Tanshinone Ⅱ A (TaHD group).The cerebral I/R models were established by the method of right middle cerebral artery occlusion (MCAO).Cerebral infarct volume was detected by TTC staining.Apoptotic cell and apoptotic index were calculated by Tunnel assay.The HMGB1 levels in brain and serum was detected by Western blot and ELISA.Calmodulin (CaM) activity and malondialdehyde (malondiadehyde,MDA) content in the brain were also detected.Results Compared with the Sham group,the volume of cerebral infarction,the number of apoptotic cells,CaM activity,MDA content,HMGB1 levels in the brain tissue and serum in group I/R,TaLD group and TaHD group increased significantly (P ＜ 0.01 ).Compared with the group I/R,the volume of cerebral infarction,the number of apoptotic cells,CaM activity,MDA content and the HMGB1 levels in brain tissue and serum in TaLD groupand TaHDgroup decreased significantly (P ＜ 0.01 ).The difference of the above index between TaLD groupand TaHDgroup was significant ( P ＜ 0.01 ).Conclusions Tan Ⅱ A could reduce the cerebral ischemic reperfusion injury in rats which was likely related with decreasing the inflammatory response in the late stage via HMGB1.
