Novel antiepileptic drug lacosamide exerts neuroprotective effects by decreasing glial activation in the hippocampus of a gerbil model of ischemic stroke.

نویسندگان

  • Ji Yun Ahn
  • Bing Chun Yan
  • Joon Ha Park
  • Ji Hyeon Ahn
  • Dae Hwan Lee
  • In Hye Kim
  • Jeong-Hwi Cho
  • Bai Hui Chen
  • Jae-Chul Lee
  • Young Shin Cho
  • Myoung Chul Shin
  • Jun Hwi Cho
  • Seongkweon Hong
  • Moo-Ho Won
  • Sung Koo Kim
چکیده

Lacosamide, which is a novel antiepileptic drug, has been reported to exert various additional therapeutic effects. The present study investigated the neuroprotective effects of lacosamide against transient cerebral ischemia-induced neuronal cell damage in the hippocampal cornu ammonis (CA)-1 region of a gerbil model. Neuronal Nuclei immunohistochemistry demonstrated that pre- and post-surgical treatment (5 min ischemia) with 25 mg/kg lacosamide protected CA1 pyramidal neurons in the lacosamide-treated-ischemia-operated group from ischemic injury 5 days post-ischemia, as compared with gerbils in the vehicle-treated-ischemia-operated group. Furthermore, treatment with 25 mg/kg lacosamide markedly attenuated the activation of astrocytes and microglia in the ischemic CA1 region at 5 days post-ischemia. The results of the present study suggested that pre- and post-surgical treatment of the gerbils with lacosamide was able to protect against transient cerebral ischemic injury-induced CA1 pyramidal neuronal cell death in the hippocampus. In addition, the neuroprotective effects of lacosamide may be associated with decreased activation of glial cells in the ischemic CA1 region.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Neuroprotective effects of novel antiepileptic drug lacosamide via decreasing glial activation in the hippocampus of a gerbil model of ischemic stroke

Results The results showed that preand post-treatment with 25 mg/kg lacosamide significantly protected neuronal death from transient cerebral ischemic injury. Many H&E positive cells, NeuN-immunoreactive neurons and a few number of F-J B-positive cells were found in the stratum pyramidale of the CA1 region in the lacosamide-treated-ischemia-operated groups compared with those in the vehicle-tre...

متن کامل

P34: Berberin Exerts Neuroprotective Effects by Modulating Pro and Anti-Inflammatory Cytokines in Rat Model of MCAO

Many complicated mechanisms are involved in brain ischemia and the role of inflammatory factors in the progression of post-ischemic injury is inevitable. In present study, anti-inflammatory effect of berberine has been investigated in reperfusion injury after acute ischemic stroke. Male Wistar rats weighing 250-270 gr were randomly divided into four cohorts: healthy rats (control, n=20), sham-o...

متن کامل

Protective Effects of Nucleobinding-2 After Cerebral Ischemia Via ‎Modulating Bcl-2/Bax Ratio and Reducing Glial Fibrillary Acid Protein ‎Expression

Introduction: Nucleobinding-2 (NUCB2) or nesfatin-1, a newly identified anorexigenic peptide, has antioxidant, anti-inflammatory, and anti-apoptotic properties. Brain ischemia-reperfusion induces irreversible damages, especially in the hippocampus area. However, the therapeutic effects of NUCB2 have not been well investigated in cerebral ischemia. This study was designed for the first time to i...

متن کامل

P1: Dextran Curcumin Promotes Novel Object Recognition Memory in Rats after Ischemic Stroke

Ischemic stroke causes the depletion of energy and induces excitotoxicity and neuroinflammation in the brain that results from thrombotic blockage. Cerebral ischemia leads to many types of memory loss, including impairment of working, spatial and object recognition memoreis. Curcumin shows strong anti-oxidoinflammatory activities but it terapathics limited by its low solubility in water and cor...

متن کامل

Neuroprotective Effect of Lacosamide on Hypoxic-Ischemic Brain Injury in Neonatal Rats

BACKGROUND AND PURPOSE Lacosamide (LCM) is an antiepileptic drug that enhances the slow inactivation of sodium channels and modulates collapsin response mediator protein-2. LCM was recently demonstrated to exert a neuroprotective effect in a murine model of traumatic brain injury and status epilepticus. Assuming the same underlying excitotoxicity-related brain injury mechanism, we hypothesized ...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Experimental and therapeutic medicine

دوره 10 6  شماره 

صفحات  -

تاریخ انتشار 2015