Butylphthalide Suppresses Neuronal Cells Apoptosis and Inhibits JNK-Caspase3 Signaling Pathway After Brain Ischemia/Reperfusion in Rats
Butylphthalide Suppresses Neuronal Cells Apoptosis and Inhibits JNK-Caspase3 Signaling Pathway After Brain Ischemia/Reperfusion in Rats
复制标题
丁苯酞抑制大鼠脑缺血/再灌注后神经元细胞凋亡并抑制 JNK-Caspase3 信号通路
DOI：
10.1007/s10571-015-0302-7
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发表时间：
2016-10-01
影响因子：
4
通讯作者：
Song, Yuan-Jian
中科院分区：
文献类型：
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作者：
Wen, Xiang-Ru;Tang, Man;Song, Yuan-Jian
虽然丁苯酞（BP）具有减少缺血诱导的脑损伤和神经元细胞死亡的保护作用，但对脑缺血/再灌注（I/R）期间发生的确切机制知之甚少。因此，本研究旨在探讨BP通过抑制c-Jun N-末端激酶（JNK）-Caspase 3信号通路对脑I/R诱导的缺血性脑损伤的神经保护机制。从Sprague-Dawley大鼠I/R后20 min开始，以15 mg/（kg/天）的剂量每天三次灌胃给予蒸馏非转基因大豆油中的BP。采用免疫组化染色和Western blotting检测海马CA 1区相关蛋白的表达，TUNEL染色检测海马CA 1区神经元凋亡率。结果表明，BP能显着保护神经元免受脑I/R引起的损伤。此外，BP组p-JNK、p-Bcl 2、p-c-Jun、FasL和cleaved-caspase 3的表达也明显降低。综上所述，BP能显著改善脑I/R损伤后海马CA 1区锥体神经元的存活，并抑制JNK-Caspase 3信号通路。
Although Butylphthalide (BP) has protective effects that reduce ischemia-induced brain damage and neuronal cell death, little is known about the precise mechanisms occurring during cerebral ischemia/reperfusion (I/R). Therefore, the aim of this study was to investigate the neuroprotective mechanisms of BP against ischemic brain injury induced by cerebral I/R through inhibition of the c-Jun N-terminal kinase (JNK)-Caspase3 signaling pathway. BP in distilled non-genetically modified Soybean oil was administered intragastrically three times a day at a dosage of 15 mg/(kg day) beginning at 20 min after I/R in Sprague-Dawley rats. Immunohistochemical staining and Western blotting were performed to examine the expression of related proteins, and TUNEL-staining was used to detect the percentage of neuronal apoptosis in the hippocampal CA1 region. The results showed that BP could significantly protect neurons against cerebral I/R-induced damage. Furthermore, the expression of p-JNK, p-Bcl2, p-c-Jun, FasL, and cleaved-caspase3 was also decreased in the rats treated with BP. In summary, our results imply that BP could remarkably improve the survival of CA1 pyramidal neurons in I/R-induced brain injury and inhibit the JNK-Caspase3 signaling pathway.