Moezi Leila, Yahosseini Siranoush, Jamshidzadeh Akram, Dastgheib Mona, Pirsalami Fateme
a Department of Pharmacology, School of Medicine , Shiraz University of Medical Sciences , Shiraz , Iran.
b Pharmaceutical Sciences Research Center , Shiraz University of Medical Sciences , Shiraz , Iran.
Neurol Res. 2018 Feb;40(2):146-152. doi: 10.1080/01616412.2017.1402500. Epub 2017 Nov 20.
Boldine is an aporphine alkaloid which is best known for its antioxidant, anti-inflammatory and cytoprotective characteristics. It seems that all these activities are related to boldine ability to scavenge reactive free radicals. As indicated by several pieces of evidence, free radicals generation are involved in initiation and propagation of epilepsy.
In this study, we investigated the sub-chronic effects of boldine on intraperitoneal and intravenous pentylenetetrazole (PTZ) models and electroshock-induced seizure in mice. Mice in treatment groups received different doses of boldine (once in a day for 8 days, ip.) and control group received solvent. We also evaluated the role of antioxidant activity of boldine as a part of its anti-seizure activity.
The results demonstrated that sub-chronic administration of boldine increased time latencies to the onset of myoclonic and clonic seizure induced by intraperitoneal PTZ model and increased clonic seizure threshold in intravenous PTZ model. It also decreased tonic hind limb extension duration in the electroshock-induced seizure model. Co-administration of boldine with a non-effective dose of vitamin C induced the anticonvulsant activity of vitamin C. Superoxide dismutase (SOD) activity in the brain tissue of animals was increased following sub-chronic administration of boldine which all indicated antioxidant activity of boldine may be a part of its anticonvulsant activity.
The anticonvulsant effects of boldine in three different animal models of epilepsy have been indicated. We have also shown that the antioxidant role of boldine might be a part of its anticonvulsant effect.
波尔定碱是一种阿朴啡生物碱,以其抗氧化、抗炎和细胞保护特性而闻名。似乎所有这些活性都与波尔定碱清除活性自由基的能力有关。有几条证据表明,自由基的产生参与癫痫的起始和传播。
在本研究中,我们研究了波尔定碱对小鼠腹腔注射和静脉注射戊四氮(PTZ)模型以及电休克诱导癫痫发作的亚慢性影响。治疗组小鼠接受不同剂量的波尔定碱(每天一次,共8天,腹腔注射),对照组接受溶剂。我们还评估了波尔定碱抗氧化活性作为其抗癫痫活性一部分的作用。
结果表明,亚慢性给予波尔定碱可延长腹腔注射PTZ模型诱发的肌阵挛和阵挛性癫痫发作的起始时间,并提高静脉注射PTZ模型的阵挛性癫痫发作阈值。它还缩短了电休克诱导癫痫发作模型中强直性后肢伸展的持续时间。将波尔定碱与无效剂量的维生素C联合使用可诱导维生素C的抗惊厥活性。亚慢性给予波尔定碱后,动物脑组织中的超氧化物歧化酶(SOD)活性增加,这均表明波尔定碱的抗氧化活性可能是其抗惊厥活性的一部分。
已表明波尔定碱在三种不同的癫痫动物模型中具有抗惊厥作用。我们还表明,波尔定碱的抗氧化作用可能是其抗惊厥作用的一部分。