Anticonvulsant Effects of Topiramate and Lacosamide on Pilocarpine-Induced Status Epilepticus in Rats: A Role of Reactive Oxygen Species and Inflammation
Status epilepticus (SE) is a neurological disorder characterized by a prolonged epileptic activity followed by subsequent epileptogenic processes. The aim of the present study was to evaluate the early effects of topiramate (TPM) and lacosamide (LCM) treatment on oxidative stress and inflammatory da...
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| Veröffentlicht in: | International journal of molecular sciences 2021-02, Vol.22 (5), p.2264 |
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| creator | Shishmanova-Doseva, Michaela Peychev, Lyudmil Yoanidu, Lyubka Uzunova, Yordanka Atanasova, Milena Georgieva, Katerina Tchekalarova, Jana |
| description | Status epilepticus (SE) is a neurological disorder characterized by a prolonged epileptic activity followed by subsequent epileptogenic processes. The aim of the present study was to evaluate the early effects of topiramate (TPM) and lacosamide (LCM) treatment on oxidative stress and inflammatory damage in a model of pilocarpine-induced SE.
Male Wistar rats were randomly divided into six groups and the two antiepileptic drugs (AEDs), TPM (40 and 80 mg/kg, i.p.) and LCM (10 and 30 mg/kg, i.p.), were injected three times repeatedly after pilocarpine administration. Rats were sacrificed 24 h post-SE and several parameters of oxidative stress and inflammatory response have been explored in the hippocampus.
The two drugs TPM and LCM, in both doses used, succeeded in attenuating the number of motor seizures compared to the SE-veh group 30 min after administration. Pilocarpine-induced SE decreased the superoxide dismutase (SOD) activity and reduced glutathione (GSH) levels while increasing the catalase (CAT) activity, malondialdehyde (MDA), and IL-1β levels compared to the control group. Groups with SE did not affect the TNF-α levels. The treatment with a higher dose of 30 mg/kg LCM restored to control level the SOD activity in the SE group. The two AEDs, in both doses applied, also normalized the CAT activity and MDA levels to control values. In conclusion, we suggest that the antioxidant effect of TPM and LCM might contribute to their anticonvulsant effect against pilocarpine-induced SE, whereas their weak anti-inflammatory effect in the hippocampus is a consequence of reduced SE severity. |
| doi_str_mv | 10.3390/ijms22052264 |
| format | Article |
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Male Wistar rats were randomly divided into six groups and the two antiepileptic drugs (AEDs), TPM (40 and 80 mg/kg, i.p.) and LCM (10 and 30 mg/kg, i.p.), were injected three times repeatedly after pilocarpine administration. Rats were sacrificed 24 h post-SE and several parameters of oxidative stress and inflammatory response have been explored in the hippocampus.
The two drugs TPM and LCM, in both doses used, succeeded in attenuating the number of motor seizures compared to the SE-veh group 30 min after administration. Pilocarpine-induced SE decreased the superoxide dismutase (SOD) activity and reduced glutathione (GSH) levels while increasing the catalase (CAT) activity, malondialdehyde (MDA), and IL-1β levels compared to the control group. Groups with SE did not affect the TNF-α levels. The treatment with a higher dose of 30 mg/kg LCM restored to control level the SOD activity in the SE group. The two AEDs, in both doses applied, also normalized the CAT activity and MDA levels to control values. In conclusion, we suggest that the antioxidant effect of TPM and LCM might contribute to their anticonvulsant effect against pilocarpine-induced SE, whereas their weak anti-inflammatory effect in the hippocampus is a consequence of reduced SE severity.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms22052264</identifier><identifier>PMID: 33668718</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Animal models ; Animals ; Anticonvulsants ; Anticonvulsants - pharmacology ; Anticonvulsants - therapeutic use ; Antiepileptic agents ; Antioxidants ; Biomarkers - metabolism ; Catalase ; Convulsions & seizures ; Cytokines ; Drug dosages ; Epilepsy ; Hippocampus ; Hippocampus - drug effects ; Hippocampus - pathology ; Hippocampus - physiopathology ; IL-1β ; Inflammation ; Inflammation - pathology ; Inflammatory response ; Interleukin-1beta - metabolism ; Lacosamide - pharmacology ; Lacosamide - therapeutic use ; Male ; Malondialdehyde ; Motor Activity - drug effects ; Oxidative stress ; Oxidative Stress - drug effects ; Pilocarpine ; Rats ; Rats, Wistar ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Seizures ; Seizures - physiopathology ; Status Epilepticus - chemically induced ; Status Epilepticus - drug therapy ; Status Epilepticus - physiopathology ; Superoxide dismutase ; Topiramate ; Topiramate - pharmacology ; Topiramate - therapeutic use ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α</subject><ispartof>International journal of molecular sciences, 2021-02, Vol.22 (5), p.2264</ispartof><rights>2021. This work is licensed under http://creativecommons.org/licenses/by/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 by the authors. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c478t-66b3768f3dbadd8fb8626f7c646531d2c51a576807d5f7792500df9e4cc930ee3</citedby><cites>FETCH-LOGICAL-c478t-66b3768f3dbadd8fb8626f7c646531d2c51a576807d5f7792500df9e4cc930ee3</cites><orcidid>0000-0003-1053-8966 ; 0000-0002-8628-167X ; 0000-0002-6423-5998 ; 0000-0001-6258-410X ; 0000-0003-1640-5099</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7956388/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7956388/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53768,53770</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33668718$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shishmanova-Doseva, Michaela</creatorcontrib><creatorcontrib>Peychev, Lyudmil</creatorcontrib><creatorcontrib>Yoanidu, Lyubka</creatorcontrib><creatorcontrib>Uzunova, Yordanka</creatorcontrib><creatorcontrib>Atanasova, Milena</creatorcontrib><creatorcontrib>Georgieva, Katerina</creatorcontrib><creatorcontrib>Tchekalarova, Jana</creatorcontrib><title>Anticonvulsant Effects of Topiramate and Lacosamide on Pilocarpine-Induced Status Epilepticus in Rats: A Role of Reactive Oxygen Species and Inflammation</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Status epilepticus (SE) is a neurological disorder characterized by a prolonged epileptic activity followed by subsequent epileptogenic processes. The aim of the present study was to evaluate the early effects of topiramate (TPM) and lacosamide (LCM) treatment on oxidative stress and inflammatory damage in a model of pilocarpine-induced SE.
Male Wistar rats were randomly divided into six groups and the two antiepileptic drugs (AEDs), TPM (40 and 80 mg/kg, i.p.) and LCM (10 and 30 mg/kg, i.p.), were injected three times repeatedly after pilocarpine administration. Rats were sacrificed 24 h post-SE and several parameters of oxidative stress and inflammatory response have been explored in the hippocampus.
The two drugs TPM and LCM, in both doses used, succeeded in attenuating the number of motor seizures compared to the SE-veh group 30 min after administration. Pilocarpine-induced SE decreased the superoxide dismutase (SOD) activity and reduced glutathione (GSH) levels while increasing the catalase (CAT) activity, malondialdehyde (MDA), and IL-1β levels compared to the control group. Groups with SE did not affect the TNF-α levels. The treatment with a higher dose of 30 mg/kg LCM restored to control level the SOD activity in the SE group. The two AEDs, in both doses applied, also normalized the CAT activity and MDA levels to control values. In conclusion, we suggest that the antioxidant effect of TPM and LCM might contribute to their anticonvulsant effect against pilocarpine-induced SE, whereas their weak anti-inflammatory effect in the hippocampus is a consequence of reduced SE severity.</description><subject>Animal models</subject><subject>Animals</subject><subject>Anticonvulsants</subject><subject>Anticonvulsants - pharmacology</subject><subject>Anticonvulsants - therapeutic use</subject><subject>Antiepileptic agents</subject><subject>Antioxidants</subject><subject>Biomarkers - metabolism</subject><subject>Catalase</subject><subject>Convulsions & seizures</subject><subject>Cytokines</subject><subject>Drug dosages</subject><subject>Epilepsy</subject><subject>Hippocampus</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - pathology</subject><subject>Hippocampus - physiopathology</subject><subject>IL-1β</subject><subject>Inflammation</subject><subject>Inflammation - pathology</subject><subject>Inflammatory response</subject><subject>Interleukin-1beta - 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The aim of the present study was to evaluate the early effects of topiramate (TPM) and lacosamide (LCM) treatment on oxidative stress and inflammatory damage in a model of pilocarpine-induced SE.
Male Wistar rats were randomly divided into six groups and the two antiepileptic drugs (AEDs), TPM (40 and 80 mg/kg, i.p.) and LCM (10 and 30 mg/kg, i.p.), were injected three times repeatedly after pilocarpine administration. Rats were sacrificed 24 h post-SE and several parameters of oxidative stress and inflammatory response have been explored in the hippocampus.
The two drugs TPM and LCM, in both doses used, succeeded in attenuating the number of motor seizures compared to the SE-veh group 30 min after administration. Pilocarpine-induced SE decreased the superoxide dismutase (SOD) activity and reduced glutathione (GSH) levels while increasing the catalase (CAT) activity, malondialdehyde (MDA), and IL-1β levels compared to the control group. Groups with SE did not affect the TNF-α levels. The treatment with a higher dose of 30 mg/kg LCM restored to control level the SOD activity in the SE group. The two AEDs, in both doses applied, also normalized the CAT activity and MDA levels to control values. In conclusion, we suggest that the antioxidant effect of TPM and LCM might contribute to their anticonvulsant effect against pilocarpine-induced SE, whereas their weak anti-inflammatory effect in the hippocampus is a consequence of reduced SE severity.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>33668718</pmid><doi>10.3390/ijms22052264</doi><orcidid>https://orcid.org/0000-0003-1053-8966</orcidid><orcidid>https://orcid.org/0000-0002-8628-167X</orcidid><orcidid>https://orcid.org/0000-0002-6423-5998</orcidid><orcidid>https://orcid.org/0000-0001-6258-410X</orcidid><orcidid>https://orcid.org/0000-0003-1640-5099</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MDPI - Multidisciplinary Digital Publishing Institute; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Animal models Animals Anticonvulsants Anticonvulsants - pharmacology Anticonvulsants - therapeutic use Antiepileptic agents Antioxidants Biomarkers - metabolism Catalase Convulsions & seizures Cytokines Drug dosages Epilepsy Hippocampus Hippocampus - drug effects Hippocampus - pathology Hippocampus - physiopathology IL-1β Inflammation Inflammation - pathology Inflammatory response Interleukin-1beta - metabolism Lacosamide - pharmacology Lacosamide - therapeutic use Male Malondialdehyde Motor Activity - drug effects Oxidative stress Oxidative Stress - drug effects Pilocarpine Rats Rats, Wistar Reactive oxygen species Reactive Oxygen Species - metabolism Seizures Seizures - physiopathology Status Epilepticus - chemically induced Status Epilepticus - drug therapy Status Epilepticus - physiopathology Superoxide dismutase Topiramate Topiramate - pharmacology Topiramate - therapeutic use Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-TNF Tumor necrosis factor-α |
| title | Anticonvulsant Effects of Topiramate and Lacosamide on Pilocarpine-Induced Status Epilepticus in Rats: A Role of Reactive Oxygen Species and Inflammation |
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