Neuroprotective Effects of Lacosamide in Experimental Peripheral Nerve Injury in Rats : A Prospective Randomized and Placebo-Controlled Trial

Demiröz, Serdar; Ur, Koray; Bengü, Aydın Şükrü; Ulucan, Aykut; Atıcı, Yunus; Erdoğan, Sinan; Çıraklı, Alper; Erdem, Şevki

doi:10.3340/jkns.2019.0178

Cited by 4 publications

(1 citation statement)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This same effect can be observed in experimentally induced transient cerebral ischemia, in which the possible neuroprotective effect of LCM on CA1 pyramidal neurons is due to the increase of CAT and GPX expression after pretreatment with LCM [43]. In two other studies, Demiroz et al [44,45] also demonstrated a neuroprotective effect of LCM after experimental peripheral nerve injury (PNI) and traumatic spinal cord injury (SCI). In both, the neuroprotective effect of LCM is linked to its ability to reduce the production of reactive oxygen species by increasing antioxidant enzyme expressions.…”

Section: Discussionmentioning

confidence: 59%

Lacosamide improves biochemical, genotoxic, and mitochondrial parameters after PTZ‐kindling model in mice

Lazzarotto

Pflüger

Regner

et al. 2020

Fundamemntal Clinical Pharma

View full text Add to dashboard Cite

This study evaluated the effect of lacosamide (LCM) on biochemical and mitochondrial parameters after PTZ kindling in mice. Male mice were treated on alternative days for a period of 11 days with LCM (20, 30, or 40 mg/kg), saline, or diazepam (2 mg/kg), before PTZ administration (50 mg/kg). The hippocampi were collected to evaluate free radicals, the activities of superoxide dismutase (SOD), catalase (CAT), and the mitochondrial complexes I‐III, II, and II‐III, as well as Bcl‐2 and cyclo‐oxygenase‐2 (COX‐2) expressions. Hippocampi, blood, and bone marrow were collected for genotoxic and mutagenic evaluations. LCM 40 mg/kg increased latency and decreased percentage of seizures, only on the 3rd day of observation. The dose of 30 mg/kg only showed positive effects on the percentage of seizures on the 2nd day of observation. LCM decreased free radicals and SOD activity and the dose of 40 mg/kg were able to increase CAT activity. LCM 30 and 40 mg/kg improved the enzymatic mitochondrial activity of the complex I‐III and LCM 30 mg/kg improved the activity of the complex II. In the comet assay, the damage induced by PTZ administration was reduced by LCM 20 and 30 mg/kg. The dose of 20 mg/kg increased COX‐2 expression while the highest dose used, 40 mg/kg, was able to reduce this expression when compared to the group treated with LCM 20 mg/kg. Although LCM did not produce the antiepileptogenic effect in vivo, it showed the neuroprotective effect against oxidative stress, bioenergetic dysfunction, and DNA damage induced by the repeated PTZ administration.

show abstract

Section: Discussionmentioning

confidence: 59%