Intraperitoneal administration of LVT decreased significantly MDA in the cortex ( KA + vehicle = 0.25 +/- 0.03 nmol/mg protein KA + LVT = 0.13 +/- 0.01 nmol/mg protein P < 0.005), and in the diencephalons ( KA + vehicle = 1,01 +/- 0.2 nmol/mg protein KA + LVT = 0,33 +/- 0,08 nmol/mg protein P < 0.005), prevented the brain loss of GSH in both cortex ( KA + vehicle = 5 +/- 1 micromol/g protein KA + LVT = 15 +/- 2 micromol/g protein P < 0.005) and diencephalons ( KA + vehicle = 9 +/- 0.8 micromol/g protein KA + LVT = 13 +/- 0.3 micromol/g protein P < 0.05), reduced brain IL-1beta mRNA and markedly controlled seizures. Animals were sacrificed 6 hours after KA injection to measure brain malonildialdehyde (MDA), glutathione levels (GSH) and the mRNA for interleukin-1beta (IL-1beta) in the cortex and in the diencephalon. Animals were randomized to receive either LVT (50 mg/kg) or its vehicle (1 ml/kg) 30 min. Sham brain injury rats were used as controls. Brain injury was induced by intraperitoneal administration of KA (10 mg/kg). We investigated the Levetiracetam (LVT) ability to protect the brain against kainic acid ( KA) induced neurotoxicity. Marini, Herbert Costa, Cinzia Passaniti, Maria Esposito, Maria Campo, Giuseppe M Ientile, Riccardo Adamo, Elena Bianca Marini, Rolando Calabresi, Paolo Altavilla, Domenica Minutoli, Letteria Pisani, Francesco Squadrito, Francesco Levetiracetam protects against kainic acid-induced toxicity. Therefore decursin is able to attenuate KA-induced seizures and could have potential as an antiepileptic drug. Furthermore, in-vivo results indicated that decursin strongly inhibits selective neuronal death, astrogliosis, and oxidative stress induced by KA administration.
The decursin-treated KA-injected group showed significantly decreased behavioral seizure activity and remarkably attenuated intense and high-frequency seizure discharges in the parietal cortex for 2 h compared with the group treated only with KA. KA injections significantly enhanced neurodegenerative conditions but treatment with decursin 30 min before KA injection reduced the detrimental effects of KA in mice. Thirty minutes after intraperitoneal injections of decursin (20 mg/kg) in male 7-week-old C57BL/6 mice, the animals were treated with KA (30 mg/kg, intraperitoneally) and then examined for behavioral seizure score, electroencephalogram, seizure-related expressed protein levels, neuronal cell loss, neurodegeneration, and astrogliosis. This study served to investigate the effects of decursin on a kainic acid ( KA)-induced status epilepticus model. Of the coumarin derivatives in Angelica gigas, decursin, a major coumarin component, was reported to exhibit significant protective activity against glutamate- induced neurotoxicity when added to primary cultures of rat cortical cells.
Lee, Jong-Keun Jeong, Ji Woon Jang, Taeik Lee, Go-Woon Han, Hogyu Kang, Jae-Seon Kim, Ik-HwanĮpilepsy is a neurological disorder with recurrent unprovoked seizures as the main symptom. Decursin attenuates kainic acid-induced seizures in mice.
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