Abstract:
: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.
journal_name
Cell Mol Neurobioljournal_title
Cellular and molecular neurobiologyauthors
Wen XR,Tang M,Qi DS,Huang XJ,Liu HZ,Zhang F,Wu J,Wang YW,Zhang XB,Guo JQ,Wang SL,Liu Y,Wang YL,Song YJdoi
10.1007/s10571-015-0302-7subject
Has Abstractpub_date
2016-10-01 00:00:00pages
1087-95issue
7eissn
0272-4340issn
1573-6830pii
10.1007/s10571-015-0302-7journal_volume
36pub_type
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