Volume 27, Issue 3 (10-2025)
yafte 2025, 27(3): 50-63 |
Back to browse issues page
Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
Shah Vali S, Rafieirad M. Effect of Auraptene on the Expression of c-Jun N-Terminal Kinase Pathway Genes in the Hippocampus of Adult Male Rats Following Cerebral Hypoperfusion Ischemia. yafte 2025; 27 (3) :50-63
URL: http://yafte.lums.ac.ir/article-1-3810-en.html
URL: http://yafte.lums.ac.ir/article-1-3810-en.html
Department of Biology, Iz.c, Islamic Azad University, Izeh, Iran & Department of Biology, Iz.c, Islamic Azad University, Izeh, Iran
Abstract: (605 Views)
Background: Cerebral hypoperfusion ischemia activates stress pathways and induces apoptosis in neurons. The JNK (MAPK8) gene, as part of oxidative stress and inflammatory pathways, plays a key role in cell death and neuronal survival. The present study sought to assess the effect of auraptene on the expression of JNK1 (MAPK8), C-fos, and C-jun genes in the hippocampus of rats subjected to cerebral hypoperfusion ischemia.
Materials and Methods: A total of 50 male Wistar rats were assigned to five groups: control, ischemia, and three ischemia groups receiving different doses of auraptene (12.5, 25, and 50 mg/kg). Ischemia was induced by bilateral carotid artery occlusion, and gene expression was measured using real-time PCR.
Results: A significant increase was observed in the expression of MAPK8, C-fos, and C-jun genes in the ischemia group compared to the control group (P<0.001). Moreover, the administration of auraptene at doses of 12.5, 25 and 50 mg/kg significantly reduced the expression of these genes compared to the ischemia group (P<0.001).
Conclusion: Auraptene probably inhibits stress and inflammatory pathways, preventing the upregulation of genes associated with ischemic injury. Furthermore, it exerts a protective effect against damage caused by cerebral hypoperfusion ischemia.
Materials and Methods: A total of 50 male Wistar rats were assigned to five groups: control, ischemia, and three ischemia groups receiving different doses of auraptene (12.5, 25, and 50 mg/kg). Ischemia was induced by bilateral carotid artery occlusion, and gene expression was measured using real-time PCR.
Results: A significant increase was observed in the expression of MAPK8, C-fos, and C-jun genes in the ischemia group compared to the control group (P<0.001). Moreover, the administration of auraptene at doses of 12.5, 25 and 50 mg/kg significantly reduced the expression of these genes compared to the ischemia group (P<0.001).
Conclusion: Auraptene probably inhibits stress and inflammatory pathways, preventing the upregulation of genes associated with ischemic injury. Furthermore, it exerts a protective effect against damage caused by cerebral hypoperfusion ischemia.
Type of Study: Original Research |
Subject:
فارماکولوژی
Received: 2025/02/9 | Accepted: 2025/07/14 | Published: 2025/10/2
Received: 2025/02/9 | Accepted: 2025/07/14 | Published: 2025/10/2
Send email to the article author
| Rights and permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
