Kaushik Dhirender, Kumar Ajay, Kaushik Pawan, Rana Avatar C
Institute of Pharmaceutical Sciences, Kurukshetra University, Kurukshetra, India.
Zhong Xi Yi Jie He Xue Bao. 2012 Sep;10(9):1056-60. doi: 10.3736/jcim20120915.
To study the anticonvulsant activity of alcoholic extract of bark of Pinus roxburghii Sarg. (AEPR) used in Indian traditional medicine system in treating convulsion.
Anticonvulsant activity was evaluated by maximal electroshock (MES) and pentylenetetrazole (PTZ)-induced seizures in Wistar albino rats. In the MES model, 150 mA current for 0.2 s was given through ear electrodes to induce convulsions in rats. The duration of tonic extension of hind limb was used as the end point, namely, prevention or decrease in the duration of hind limb extension was considered as a protective action. In the PTZ model, the anticonvulsant property of AEPR was assessed by its ability to delay the onset of myoclonic spasm and clonic convulsions produced by intraperitoneal administration of PTZ.
In the MES-induced seizure model, AEPR in doses of 300 and 500 mg/kg body weight reduced all the phases of convulsion significantly (P<0.01). Standard drug phenytoin at a dose of 25 mg/kg significantly reduced flexion phase (P<0.01) and abolished all phases of convulsion. In the PTZ-induced seizure model, the administration of the extract at doses of 300 and 500 mg/kg 30 min prior to injection of PTZ significantly delayed the onset of clonic seizure (P<0.01). AEPR at the dose of 100 mg/kg body weight could not exert any significant protective effect on PTZ-induced convulsions. Standard drug diazepam at a dose of 4 mg/kg showed much delayed onset of clonic seizure.
The study suggests that AEPR would be effective against generalized tonic-clonic and partial seizures. Thus AEPR possesses anticonvulsant property against MES- and PTZ-induced seizures in Wistar rats. However, further research is in progress to isolate the compound responsible for its activity.
研究印度传统医学体系中用于治疗惊厥的喜马拉雅松（Pinus roxburghii Sarg.）树皮乙醇提取物（AEPR）的抗惊厥活性。
通过最大电休克（MES）和戊四氮（PTZ）诱导Wistar白化大鼠惊厥来评估抗惊厥活性。在MES模型中，通过耳部电极给予150 mA电流持续0.2 s以诱导大鼠惊厥。将后肢强直性伸展的持续时间作为终点，即后肢伸展持续时间的预防或减少被视为一种保护作用。在PTZ模型中，通过AEPR延迟腹腔注射PTZ引起的肌阵挛性痉挛和阵挛性惊厥发作的能力来评估其抗惊厥特性。
在MES诱导的惊厥模型中，体重剂量为300和500 mg/kg的AEPR显著降低了惊厥的所有阶段（P<0.01）。剂量为25 mg/kg的标准药物苯妥英显著降低了屈曲期（P<0.01）并消除了惊厥的所有阶段。在PTZ诱导的惊厥模型中，在注射PTZ前30分钟给予300和500 mg/kg剂量的提取物显著延迟了阵挛性惊厥的发作（P<0.01）。体重剂量为100 mg/kg的AEPR对PTZ诱导的惊厥没有任何显著的保护作用。剂量为4 mg/kg的标准药物地西泮显示阵挛性惊厥发作的延迟时间更长。
该研究表明AEPR对全身性强直阵挛性发作和部分性发作有效。因此，AEPR对Wistar大鼠的MES和PTZ诱导的惊厥具有抗惊厥特性。然而，正在进行进一步的研究以分离负责其活性的化合物。
