CAJ | 학술논문

目的：探讨丹参酮IIA对大鼠局灶性脑缺血再灌注后细胞凋亡、Drp-1、TRPM7表达的影响。方法分别用高低剂量丹参酮IIA预处理大鼠，制备局灶性脑缺血模型，缺血2 h后开始监测缺血区大脑中动脉脑血流变化直到再灌注24 h，2,3,5-氯化三苯基四氮唑(2,3,5-triphenyltetrazolium chloride，TTC)染色法检测脑梗死体积，原位末端标记(in situ nick-end labeling，TUNEL)检测神经元凋亡，免疫组化及Western blot检测发动相关蛋白-1（dynamin-related protein 1，Drp-1）、瞬时受体电位离子通道蛋白7（transient Receptor Potential cation chan-nel7，TRPM7）蛋白表达水平。结果丹参酮IIA高低剂量组能明显抑制缺血区脑组织Drp-1及TRPM7蛋白表达(P<0.05)，减少凋亡细胞数(P<0.05)，缩小脑梗死体积(P<0.05)。缺血2 h后再灌注24 h, I/R组右侧大脑中动脉缺血区血流量下降为31.80%±2.49%，与I/R组比较，I/R+Tan1组及I/R+Tan2组血流量分别为（54.8%±3.27%）、（58.8%±3.03%），P<0.05，但丹参酮IIA高低剂量组两者之间的脑梗死体积、TUNEL阳性细胞数、对脑血流量的改善无差异性(P>0.05)。结论丹参酮IIA对大鼠局灶性脑缺血再灌注后神经元凋亡及线粒体裂解有抑制作用，其机制可能与改善缺血区脑血流量，减少Drp-1、TRPM7表达有关。
목적：탐토단삼동IIA대대서국조성뇌결혈재관주후세포조망、Drp-1、TRPM7표체적영향。방법분별용고저제량단삼동IIA예처리대서，제비국조성뇌결혈모형，결혈2 h후개시감측결혈구대뇌중동맥뇌혈류변화직도재관주24 h，2,3,5-록화삼분기사담서(2,3,5-triphenyltetrazolium chloride，TTC)염색법검측뇌경사체적，원위말단표기(in situ nick-end labeling，TUNEL)검측신경원조망，면역조화급Western blot검측발동상관단백-1（dynamin-related protein 1，Drp-1）、순시수체전위리자통도단백7（transient Receptor Potential cation chan-nel7，TRPM7）단백표체수평。결과단삼동IIA고저제량조능명현억제결혈구뇌조직Drp-1급TRPM7단백표체(P<0.05)，감소조망세포수(P<0.05)，축소뇌경사체적(P<0.05)。결혈2 h후재관주24 h, I/R조우측대뇌중동맥결혈구혈류량하강위31.80%±2.49%，여I/R조비교，I/R+Tan1조급I/R+Tan2조혈류량분별위（54.8%±3.27%）、（58.8%±3.03%），P<0.05，단단삼동IIA고저제량조량자지간적뇌경사체적、TUNEL양성세포수、대뇌혈류량적개선무차이성(P>0.05)。결론단삼동IIA대대서국조성뇌결혈재관주후신경원조망급선립체렬해유억제작용，기궤제가능여개선결혈구뇌혈류량，감소Drp-1、TRPM7표체유관。
Objective To explore the effect of Tanshinone IIA on apoptosis and expression of Drp-1 and TRPM7 in a rat model of focal cerebral ischemia and reperfusion. Methods Rats were pretreated with high or low dose of tanshinone IIA before 2 h-focal cerebral ischemia plus 24 h-reperfusion. Cerebral blood flow in the middle cerebral artery was moni-tored during reperfusion. TTC, TUNEL and western blotting were used to detect the volume of cerebral infarction, apopto-sis and the protein expression of Drp-1 as well as TRPM7, respectively. Results Compared with control group, pretreat-ment with Tanshinone IIA could significantly down-regulate the expression of protein Drp-1 and TRPM7 (P<0.05), attenu-ate apoptosis (P<0.05), and reduce the volume of ischemia infarction. The volumes of right middle cerebral artery blood flow were(31.80%± 2.49%),(54.8%± 3.27%), and(58.8%± 3.03%)in controls, low-dose and high dose of tanshinone, respectively. Both low-dose and high-dose tanshinones improved cerebral blood flow. (tanshinone vs. control;all P<0.05). However, there was no statistical difference between low-dose and high-dose Tanshinone IIA groups in all measured out-comes (P>0.05). Conclusions Tanshinone IIA can inhibit ischemia-induced neuronal apoptosis and mitochondrial fission probably through improving cerebral artery blood flow and reducing the overexpression of Drp-1,TRPM7.