李琴 韩力培 李泽慧 张均田 唐民科. 丹酚酸B通过抑制MAPK通路减轻大鼠脑缺血再灌注引起的血脑屏障损伤J. 药学学报, 2010,45(12): 1485-1490.
引用本文: 李琴 韩力培 李泽慧 张均田 唐民科. 丹酚酸B通过抑制MAPK通路减轻大鼠脑缺血再灌注引起的血脑屏障损伤J. 药学学报, 2010,45(12): 1485-1490.
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LI Qin, HAN Li-Pei, LI Ze-Hui, ZHANG Jun-Tian, TANG Min-Ke. Salvianolic acid B alleviate the disruption of blood-brain barrier in rats after cerebral ischemia-reperfusion by inhibiting MAPK pathwayJ. 药学学报, 2010,45(12): 1485-1490.
Citation: LI Qin, HAN Li-Pei, LI Ze-Hui, ZHANG Jun-Tian, TANG Min-Ke. Salvianolic acid B alleviate the disruption of blood-brain barrier in rats after cerebral ischemia-reperfusion by inhibiting MAPK pathwayJ. 药学学报, 2010,45(12): 1485-1490.
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丹酚酸B通过抑制MAPK通路减轻大鼠脑缺血再灌注引起的血脑屏障损伤

Salvianolic acid B alleviate the disruption of blood-brain barrier in rats after cerebral ischemia-reperfusion by inhibiting MAPK pathway

    摘要
  • 摘要:

    本研究旨在观察丹酚酸B对脑缺血再灌注损伤大鼠血脑屏障的影响, 探讨其可能的作用机制。研究采用线栓法阻塞大鼠大脑中动脉, 并于缺血后2 h进行再灌注, 造成脑缺血再灌注损伤, 用免疫组织化学法检测缺血侧脑血管周围免疫球蛋白IgG的渗出以及MMP-9 (基质金属蛋白酶-9) 和NOS2 (一氧化氮合酶2) 的表达, 用Western blotting方法检测p-p38和p-ERK1/2蛋白含量变化。结果显示, 手术后第2天缺血再灌注组损伤侧脑血管周围免疫球蛋白IgG的渗出增加, 表明血脑屏障功能破坏, 脑组织中MMP-9和NOS2表达增加, 同时p-p38和p-ERK1/2含量也明显增加。手术后第7天, 缺血再灌注组脑组织中MMP-9及NOS2依然维持在同手术后第2天接近的高水平, p-p38含量高于手术后第2天, p-ERK1/2含量略低于手术后第2天。丹酚酸B (1和10 mg·kg−1) 能够明显改善缺血再灌注引起IgG的渗出增加 (P < 0.05), 同时MMP-9和NOS2表达也明显抑制 (P < 0.05)。丹酚酸B (10 mg·kg−1) 能够显著降低手术后第2天和第7天p-p38和p-ERK1/2蛋白含量 (P < 0.05)。丹酚酸B (1 mg·kg−1) 在手术后第7天能显著减少p-p38的含量 (P < 0.05)。以上结果表明, 丹酚酸B的血脑屏障保护作用可能与抑制MMP-9激活相关, 其中丹酚酸B抑制MAPK通路可能起重要作用。

     

    Abstract:

    The aim of the study is to investigate the effect of salvianolic acid B (SalB) on blood-brain barrier (BBB) in rats after cerebral ischemia-reperfusion, and to illustrate its possible mechanisms.  Cerebral ischemia- reperfusion was induced by middle cerebral artery occlusion in rats.  The break-down of BBB was indicated by extravasations of immunoglobulin (IgG) monitored with immunohistochemistry.  The expression of MMP-9 and NOS2 in the brain was determined by immunohistochemistry, and the expression of p-p38 and p-ERK1/2 was detected by Western blotting.  It was shown that on day 2 after ischemia-reperfusion the IgG accumulated around the vascular boundary zone, suggesting the break-down of BBB, and the expression of MMP-9 and NOS2 up-regulated at the same time.  The result of Western blotting suggested that the expression of p-p38 and p-ERK1/2 increased.  On day 7 after ischemia-reperfusion the expression of MMP-9 and NOS2 was about the same level as day 2, the expression of p-p38 was higher than that on day 2 and the expression of p-ERK1/2   was slightly lower than that on day 2.  SalB (1 and 10 mg·kg−1) significantly alleviated the extravasations of immunoglobulin induced by cerebral ischemia-reperfusion (P < 0.05).  On day 2 and day 7 SalB attenuated the expression of MMP-9 and NOS2 (P < 0.05).  SalB (10 mg·kg−1) reduced the expression of p-p38 and p-ERK1/2 apparently on day 2 and 7 after ischemia-reperfusion (P < 0.05).  SalB (1 mg·kg−1) inhibited the expression of p-p38 on day 7 after ischemia-reperfusion (P < 0.05).  The results indicate that SalB protects blood-brain barrier in rats after cerebral ischemia-reperfusion by inhibiting the MAPK pathway.

     

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