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目的:初步探讨核因子-κB(nuclear factor κB,NF-κB)与细胞间黏附分子-1(intercellular adhension molecule-1,ICAM-1)在实验性高血压脑出血阳类证的病证结合模型鼠脑损伤中的作用及其可能的参与途径,推测益脑脉胶囊对出血中风阳类证可能的神经保护机制。方法:采用双肾双夹、脑内注入胶原酶、灌服热性药物煎剂以及复方地芬诺酯(Compound Diphennoxylate,CD)法复制高血压脑出血阳类证病证结合模型鼠。采用免疫组化、原位杂交法分别检测各组大鼠造模后6、12、24、48h,3天5个时间点右侧尾状核区(血肿周围脑组织)NF-κB的活性以及ICAM-1mRNA的表达变化,并观察益脑脉胶囊对上述指标的影响。结果:脑出血术后,右侧尾状核区NF-κB和ICAM-1mRNA的表达分别在6,12h即明显升高,分别在12,48h达到高峰,3天仍高于正常对照组(P均<0.01)。在各对应时间点,益脑脉胶囊治疗可降低NF-κB和ICAM-1mRNA的活性(P<0.05或P<0.01)。结论:NF-κB、ICAM-1可能参与了脑出血后血肿周围的损害过程;益脑脉胶囊可能通过抑制NF-κB的活性,下调ICAM-1mRNA的表达,从而发挥脑保护作用。
OBJECTIVE: To investigate the combination of pathological and spermatozoa of experimental type of hypertensive intracerebral hemorrhage (ICH) with positive sign of nuclear factor κB (NF-κB) and intercellular adhesion molecule-1 (ICAM-1) The role of brain injury in rats and its possible ways of participation, presumably Yibaomai capsule on hemorrhagic stroke Yang card potential neuroprotective mechanisms. Methods: Duplicate model of renal hypertensive intracerebral hemorrhage was established by injecting collagenase, intracerebral injection of collagenase, decoction of thermal drugs and compound Diphennoxylate (CD). Immunohistochemistry and in situ hybridization were used to detect the activity of NF-κB in the right caudate nucleus caudatum (brain around hematoma) at 6, 12, 24, 48 and 3 days after modeling ICAM-1mRNA expression changes, and observe the effect of Yitaimai capsule on the above indicators. Results: After cerebral hemorrhage, the expression of NF-κB and ICAM-1 mRNA in the right caudate nucleus significantly increased at 6 and 12 h, respectively, reaching the peak at 12 and 48 h respectively and still higher than that of the normal control group at 3 days (P All <0.01). At each time point, treatment with Yitaimai Capsule reduced the activity of NF-κB and ICAM-1 mRNA (P <0.05 or P <0.01). CONCLUSION: NF-κB and ICAM-1 may be involved in the process of perihematoma injury after intracerebral hemorrhage. Yitaimai capsule may play a protective role by inhibiting the activity of NF-κB and down-regulating the expression of ICAM-1 mRNA.