TY - JOUR AB - The aim of the present study was to investigate the influence of butylphthalide on nerve cell apoptosis in rats with cerebral infarction through the c‑Jun N‑terminal kinase (JNK)/p38 mitogen‑activated protein kinase (MAPK) signaling pathway. A total of 36 Sprague‑Dawley rats were randomly divided into sham‑operation group (n=12), model group (n=12) and butylphthalide group (n=12). Additionally, qPCR was performed to measure the mRNA expression of Bax and Bcl‑2, and a TUNEL assay was conducted to investigate the cell apoptosis. Compared with the sham‑operation group, the model group and the butylphthalide group had notably increased Zea‑Longa scores (P<0.05), while the butylphthalide group exhibited a markedly decreased Zea‑Longa score, compared with the model group (P<0.05). The positive expression of Bax was markedly higher (P<0.05), while that of Bcl‑2 was notably lower in the model group and the butylphthalide group (P<0.05), compared with those in the sham‑operation group. Furthermore, the positive expression of Bax was notably decreased (P<0.05), while that of Bcl‑2 was markedly increased in the butylphthalide group in comparison with those in model group (P<0.05). The model group and the butylphthalide group had markedly higher relative protein expression levels of p‑JNK and p‑p38 MAPK than the sham‑operation group (P<0.05), and the butylphthalide group displayed notably lower relative protein expression levels of p‑JNK and p‑p38 MAPK than the model group (P<0.05). The relative mRNA expression level of Bax was markedly increased (P<0.05), while that of Bcl‑2 was notably decreased in the model group and the butylphthalide group (P<0.05), compared with those in the sham‑operation group. Compared with those in the model group, the relative mRNA expression level of Bax decreased markedly (P<0.05), and that of Bcl‑2 increased notably in the butylphthalide group (P<0.05). The apoptotic rate was markedly higher in the model group and the butylphthalide group than that in the sham‑operation group (P<0.05), but it was notably lower in the butylphthalide group than that in the model group (P<0.05). In conclusion, butylphthalide may inhibit nerve cell apoptosis in rats with cerebral infarction to exert a protective effect, which may be associated with the JNK/p38 MAPK signaling pathway. AD - Department of Geratology Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310000, P.R. China Department of Neurology, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310000, P.R. China Department of Geratology, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310000, P.R. China AU - Bu,Xiangye AU - Xia,Wenqing AU - Wang,Xiaonan AU - Lu,Shan AU - Gao,Yue DA - 2021/06/01 DO - 10.3892/etm.2021.9997 IS - 6 JO - Exp Ther Med KW - butylphthalide cerebral infarction JNK/p38 MAPK signaling pathway apoptosis PY - 2021 SN - 1792-0981 1792-1015 SP - 565 ST - Butylphthalide inhibits nerve cell apoptosis in cerebral infarction rats via the JNK/p38 MAPK signaling pathway T2 - Experimental and Therapeutic Medicine TI - Butylphthalide inhibits nerve cell apoptosis in cerebral infarction rats via the JNK/p38 MAPK signaling pathway UR - https://doi.org/10.3892/etm.2021.9997 VL - 21 ER -