Tenoxicam mitigates nuclear factor kappa B gene expression level in the male Wistar rats’ model of the seizures
کد: G-1039
نویسندگان: Nasrin Abdollahzadeh ℗, Zahra Guilandokht, Zahra Nazari, Bita Amiri Hazaveh, Solmaz Jamshidi Dolat Abad, Saghi Hakimi Naeini , Abdolkarim Hosseini, Vahid Azizi ©
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خلاصه مقاله:
background
Seizures are known to induce significant neuronal damage and provoke an inflammatory response within the brain. The nuclear factor-kappa B (NF-κB) pathway is a crucial mediator of inflammation, and its activation has been implicated in seizure-related neuroinflammation. This study investigates the efficacy of Tenoxicam (TNX), a widely used nonsteroidal anti-inflammatory drug (NSAID), in modulating NF-κB activity and reducing inflammation in the brain of rats subjected to pentylenetetrazole (PTZ)-induced seizures.
Methods
The total of 24 male Wistar rats were randomly assigned to four groups: a control group, a PTZ group and the TNX treatment groups. Seizures were induced via intraperitoneal injection of PTZ in groups. The TNX group received an intraperitoneal injection of TNX (dosage: 0.6 and 1.2 mg/kg) 30 min prior to PTZ administration. Brain tissues were collected post-seizure induction for analysis. NF-κB expression were quantified using Real-Time PCR.
Findings
The PTZ group, which did not receive TNX, demonstrated a pronounced inflammatory response, characterized by significantly elevated NF-κB expression compared to the control group (P0.001). In contrast, animals administered TNX exhibited a marked attenuation of NF-κB expression, indicating a considerable reduction in neuroinflammatory activity relative to the PTZ group (P0.001).
Conclusion
This study demonstrates that TNX significantly reduces NF-κB expression and neuroinflammation in rats subjected to PTZ-induced seizures, supporting its potential as a neuroprotective agent. By attenuating the inflammatory response, TNX may help mitigate seizure-induced neuronal damage.
Key words
NSAID; Tenoxicam; Seizures