Apelina-13 hamuje zawały o wysokiej częstotliwości związane z napadami oraz zmniejsza uszkodzenia neuroinflammacyjne w ostrym modelu epilepsji indukowanej pentylenotetrazolem u szczurów

The Apelin-13/APJ system exerts anti-excitatory, antioxidant, and anti-inflammatory effects in the central nervous system, however, its influence on seizure-associated pathological high-frequency oscillations (HFOs) and concurrent neuroinflammatory tissue injury has not been investigated in vivo. This study evaluated the effects of intracerebroventricular Apelin-13 pretreatment on seizure severity, cortical electrophysiology, and neuroinflammatory injury in a pentylenetetrazol (PTZ)-induced acute rat epilepsy model. Thirty adult male Wistar rats were assigned to three groups (n = 10): Control, PTZ (70 mg/kg, i.p.), and APL + PTZ (Apelin-13 3 μg/5 μl, i.c.v., 15 min prior to PTZ). Seizure severity was scored using the Racine scale. Cortical EEG was recorded via epidural electrodes and analyzed by power spectral density across six bands. Brain sections were evaluated by haematoxylin-eosin staining, TUNEL assay, and eNOS/VEGF immunohistochemistry. Apelin-13 significantly reduced seizure severity (p < 0.05). PTZ elevated cortical power across all frequency bands. Apelin-13 attenuated power in the theta, alpha, gamma, and HFO bands (p < 0.05 to p < 0.01), with the strongest suppression in the HFO band (p < 0.01), where APL + PTZ values were indistinguishable from controls. Apelin-13 reduced the neuronal damage score (p < 0.01), apoptotic index (p < 0.05), eNOS expression (p < 0.01), and VEGF expression (p < 0.001). These findings indicate that Apelin-13 suppresses seizure-associated HFO activity and attenuates convergent nitrosative, apoptotic, and vascular injury pathways in acute PTZ-induced epilepsy, supporting the Apelin-13/APJ axis as a mechanistically distinct neuroprotective candidate warranting further translational investigation.