The effect of flunixin meglumine on nuclear factor kappa B gene expression in the male Wistar rats’ model of the seizures
کد: G-1040
نویسندگان: Sina Amiribesheli ℗, Sepideh Saeidinia, Armaghan Rahimzade, Leili Memarzadeh, Anahita Abravan, Seyedeh Romina Lavasani, Abdolkarim Hosseini, Vahid Azizi ©
زمان بندی: زمان بندی نشده!
دانلود: دانلود پوستر
خلاصه مقاله:
background
Epilepsy is a prevalent neurological disorder, and the relationship between seizures and the expression of the nuclear factor kappa B (NF-κB) gene is of considerable importance in neurobiology. NF-κB is a critical transcription factor involved in regulating inflammatory pathways, and during seizures, its gene expression is often elevated, increasing the production of pro-inflammatory cytokines and chemokines that can lead to neuronal damage. This study aims to evaluate the effect of flunixin meglumine (FM) on NF-κB gene expression in a PTZ-induced seizure model in male Wistar rats.
Methods
A total of 24 male Wistar rats ( 200-250 g, 8 weeks old) were randomly allocated into four groups (n=6). The treatment groups were administered intraperitoneal (IP) injections of FM at doses of 1.1 and 2.2 mg/kg, while the control and PTZ groups received physiological saline. Thirty minutes post-treatment, the animals received an IP injection of PTZ at a dose of 60 mg/kg to induce seizures. Afterward, the rats were anesthetized, and brain tissue was harvested and immediately frozen at -80°C for subsequent analysis. NF-κB gene expression levels were quantified using real-time PCR.
Findings
The results demonstrated a significant upregulation of NF-κB gene expression in the PTZ group compared to the control group (p0.001). Notably, the groups treated with FM exhibited a significant reduction in NF-κB expression relative to the PTZ group (p0.001).
Conclusion
FM reduced NF-κB gene expression. The downregulation of NF-κB gene expression observed in FM-treated animals highlights the therapeutic potential of this drug in mitigating seizure-induced inflammation and neuronal damage.
Key words
Nonsteroidal anti-inflammatory drug
