<p>Ganoderma lucidum extract (GLE) has neuro-therapeutic and anticonvulsant effects. This study aimed to evaluate the potential neuroprotective and antioxidant effects of ethanolic extract on pentylenetetrazol-induced brain damage in male Wistar rats and to analyze behavioral manifestations in vivo. Seizure latency, duration, and severity were measured in PTZ-treated rats according to the Racine scale; thus, oxidative stress markers, malondialdehyde (MDA), nitric oxide (NO), and catalase catalytic activity were measured by the 2-thiobarbituric acid, Griess reagent, and hydrogen peroxide methods, respectively. PTZ-injured rats showed both shorter seizure latency and longer seizure duration and intense seizure severity. The effects were enhanced by GLE in a dose-dependent manner. In addition, GLE decreased NO levels, increased catalase levels and decreased MDA levels in the hippocampus and the prefrontal cortex in rats treated with PTZ (75&#xa0;mg/kg; i.p.). GLE conferred anticonvulsant and neuroprotective effects against PTZ-induced brain damage by repressing molecular processes involved in the production of oxidative stress markers.</p> Graphical Abstract <p></p>

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Evaluation of the Potential Anticonvulsant and Neuroprotective Effects of Ganoderma Lucidum Extract in an Animal Model of Pentylenetetrazol-Induced Seizures

  • Itto Rahou Abdessamad,
  • El-Hessni Aboubaker,
  • Bahbiti Youssef,
  • Bikjdaouene Leila,
  • Azeroil Fatima,
  • El Mekhlouf Youssef,
  • Ibouzine-Dine Laila,
  • Mesfioui Abdelhalem

摘要

Ganoderma lucidum extract (GLE) has neuro-therapeutic and anticonvulsant effects. This study aimed to evaluate the potential neuroprotective and antioxidant effects of ethanolic extract on pentylenetetrazol-induced brain damage in male Wistar rats and to analyze behavioral manifestations in vivo. Seizure latency, duration, and severity were measured in PTZ-treated rats according to the Racine scale; thus, oxidative stress markers, malondialdehyde (MDA), nitric oxide (NO), and catalase catalytic activity were measured by the 2-thiobarbituric acid, Griess reagent, and hydrogen peroxide methods, respectively. PTZ-injured rats showed both shorter seizure latency and longer seizure duration and intense seizure severity. The effects were enhanced by GLE in a dose-dependent manner. In addition, GLE decreased NO levels, increased catalase levels and decreased MDA levels in the hippocampus and the prefrontal cortex in rats treated with PTZ (75 mg/kg; i.p.). GLE conferred anticonvulsant and neuroprotective effects against PTZ-induced brain damage by repressing molecular processes involved in the production of oxidative stress markers.

Graphical Abstract