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Capsaicin Exerts Anti-convulsant and Neuroprotective Effects in Pentylenetetrazole-Induced Seizures.
Neurochemical Research ( IF 3.7 ) Pub Date : 2020-02-08 , DOI: 10.1007/s11064-020-02979-3
Omar M E Abdel-Salam 1 , Amany A Sleem 2 , Marawan Abd El Baset Mohamed Sayed 2 , Eman R Youness 3 , Nermeen Shaffie 4
Affiliation  

The transient receptor potential vanilloid-1 (TRPV1) receptor has been implicated in the development of epileptic seizures. We examined the effect of the TRPV1 agonist capsaicin on epileptic seizures, neuronal injury and oxidative stress in a model of status epilepticus induced in the rat by intraperitoneal (i.p.) injections of pentylenetetrazole (PTZ). Capsaicin was i.p. given at 1 or 2 mg/kg, 30 min before the first PTZ injection. Other groups were i.p. treated with the vehicle or the anti-epileptic drug phenytoin (30 mg/kg) alone or co-administered with capsaicin at 2 mg/kg. Brain levels of malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide, and paraoxonase-1 (PON-1) activity, seizure scores, latency time and PTZ dose required to reach status epilepticus were determined. Histopathological assessment of neuronal damage was done. Results showed that brain MDA decreased by treatment with capsaicin, phenytoin or capsaicin/phenytoin. Nitric oxide decreased by capsaicin or capsaicin/phenytoin. GSH and PON-1 activity increased after capsaicin, phenytoin or capsaicin/phenytoin. Mean total seizure score decreased by 48.8% and 66.3% by capsaicin compared with 78.7% for phenytoin and 69.8% for capsaicin/phenytoin treatment. Only phenytoin increased the latency (115.7%) and threshold dose of PTZ (78.3%). Capsaicin did not decrease the anti-convulsive effect of phenytoin but prevented the phenytoin-induced increase in latency time and threshold dose. Neuronal damage decreased by phenytoin or capsaicin at 2 mg/kg but almost completely prevented by capsaicin/phenytoin. Thus in this model of status epilepticus, capsaicin decreased brain oxidative stress, the severity of seizures and neuronal injury and its co-administration with phenytoin afforded neuronal protection.

中文翻译:

辣椒素在戊四唑诱发的癫痫发作中具有抗惊厥和神经保护作用。

瞬态受体电位香草酸-1(TRPV1)受体已牵涉癫痫发作的发展。我们在腹膜内(ip)注射戊四氮(PTZ)诱导的大鼠癫痫持续状态模型中研究了TRPV1激动剂辣椒素对癫痫发作,神经元损伤和氧化应激的影响。在第一次PTZ注射前30分钟,以1或2 mg / kg的剂量腹膜内给予辣椒素。其他组单独用溶媒或抗癫痫药苯妥英钠(30 mg / kg)或与2 mg / kg辣椒素共同给药进行腹膜内治疗。确定了达到癫痫持续状态所需的脑中丙二醛(MDA),还原型谷胱甘肽(GSH),一氧化氮和对氧磷酶-1(PON-1)活性的水平,癫痫发作评分,潜伏时间和PTZ剂量。对神经元损伤进行了组织病理学评估。结果显示,通过辣椒素,苯妥英钠或辣椒素/苯妥英钠治疗可降低脑MDA。辣椒素或辣椒素/苯妥英钠减少一氧化氮。辣椒素,苯妥英钠或辣椒素/苯妥英钠后,GSH和PON-1活性增加。辣椒素的平均总癫痫发作评分分别下降了48.8%和66.3%,苯妥英钠为78.7%,辣椒素/苯妥英钠为69.8%。仅苯妥英钠增加了潜伏期(115.7%)和PTZ阈值剂量(78.3%)。辣椒素没有降低苯妥英的抗惊厥作用,但阻止了苯妥英诱导的潜伏时间和阈值剂量的增加。苯妥英钠或辣椒素的浓度为2 mg / kg时,神经元损伤减少,但辣椒素/苯妥英钠几乎可以完全防止神经损伤。因此,在这种癫痫持续状态模型中,辣椒素减少了脑部的氧化应激,
更新日期:2020-02-10
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