Salidroside shows anticonvulsant and neuroprotective effects by activating the Nrf2-ARE pathway in a pentylenetetrazol-kindling epileptic model.

Evidence points towards oxidative stress and neuroinflammation being major processes associated with brain dysfunction in epilepsy. Salidroside reportedly possesses anti-oxidative activity and neuroprotective potential, in addition to exerting an anti-neuroinflammatory response. This study was designed to evaluate the anticonvulsant and neuroprotective role of salidroside in rats with pentylenetetrazole (PTZ) kindling and to explore the underlying mechanism. Male Wistar rats were administered a sub-convulsive dose of PTZ (35 mg/kg) every other day for 15 injections, and salidroside (50 mg/kg) was injected intraperitoneally along with alternate-day PTZ. The seizure degree, cognitive function, and number of hippocampal neurons were investigated. The expression of nuclear factor erythroid 2-related factor- antioxidant response element (Nrf2-ARE) signaling pathways, oxidative stress parameters and inflammatory cytokines were also observed. Our study showed that salidroside treatment suppressed the kindling acquisition process, ameliorated cognitive impairment, and rescued the number of pyramidal neurons in the CA3 regions. Salidroside treatment could activate the Nrf2-ARE signal pathway, and suppressed oxidative stress and neuroinflammation. Our findings demonstrated that salidroside exerted anticonvulsant and neuroprotective effects in epileptic rats by activating the Nrf2-ARE signal pathway.