Open Access

Butylphthalide inhibits nerve cell apoptosis in cerebral infarction rats via the JNK/p38 MAPK signaling pathway

  • Authors:
    • Xiangye Bu
    • Wenqing Xia
    • Xiaonan Wang
    • Shan Lu
    • Yue Gao
  • View Affiliations

  • Published online on: March 26, 2021     https://doi.org/10.3892/etm.2021.9997
  • Article Number: 565
  • Copyright: © Bu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

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.
View Figures
View References

Related Articles

Journal Cover

June-2021
Volume 21 Issue 6

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Bu X, Xia W, Wang X, Lu S and Gao Y: Butylphthalide inhibits nerve cell apoptosis in cerebral infarction rats via the JNK/p38 MAPK signaling pathway. Exp Ther Med 21: 565, 2021
APA
Bu, X., Xia, W., Wang, X., Lu, S., & Gao, Y. (2021). Butylphthalide inhibits nerve cell apoptosis in cerebral infarction rats via the JNK/p38 MAPK signaling pathway. Experimental and Therapeutic Medicine, 21, 565. https://doi.org/10.3892/etm.2021.9997
MLA
Bu, X., Xia, W., Wang, X., Lu, S., Gao, Y."Butylphthalide inhibits nerve cell apoptosis in cerebral infarction rats via the JNK/p38 MAPK signaling pathway". Experimental and Therapeutic Medicine 21.6 (2021): 565.
Chicago
Bu, X., Xia, W., Wang, X., Lu, S., Gao, Y."Butylphthalide inhibits nerve cell apoptosis in cerebral infarction rats via the JNK/p38 MAPK signaling pathway". Experimental and Therapeutic Medicine 21, no. 6 (2021): 565. https://doi.org/10.3892/etm.2021.9997