Impact of noscapine on halting the progression of pentylenetetrazole induced kindling epilepsy in mice
| dc.contributor.author | Gupta, Rishav | |
| dc.contributor.author | Soni, Divya | |
| dc.contributor.author | Upadhayay, Shubham | |
| dc.contributor.author | Dhureja, Maanvi | |
| dc.contributor.author | Kumar, Puneet | |
| dc.date.accessioned | 2024-01-21T10:55:18Z | |
| dc.date.accessioned | 2024-08-14T07:44:16Z | |
| dc.date.available | 2024-01-21T10:55:18Z | |
| dc.date.available | 2024-08-14T07:44:16Z | |
| dc.date.issued | 2023-09-19T00:00:00 | |
| dc.description.abstract | Epilepsy is caused by an excessive recurrent excitatory neuronal firing, characterized by motor, psychomotor, and sensory impairments. Current therapies fail to produce 100% outcomes because of the complexity of the disease, poor diagnosis, and upsurge�to drug-resistant epilepsy. The study repurposed�the drug �noscapine��mainly known for its anti-tussive properties. For the management of epilepsy and its associated secondary complications. To confirm the effect of noscapine, adult mice were injected with pentylenetetrazole (PTZ) (35 mg/kg i.p.) on an alternate day for 29 days to induce epilepsy. Animals were pretreated with noscapine in three doses (5, 10, and 20 mg/kg i.p.) for 33 days. Various behavioural assessments like the open field test, Morris water maze, and tail suspension test were performed to observe animals' locomotor activity, spatial memory, and anxiety-depressive behaviour. On the 34th day, animals were sacrificed, and brains were removed for biochemical estimations. Prolonged PTZ treatment reduced locomotor, learning activity, and increased anxiety-depressive behaviour, which was further confirmed by reduced antioxidant levels such as reduced glutathione (GSH), superoxide dismutase (SOD), and catalase because of increased oxido-nitrosative stress, that is, malondialdehyde (MDA) and nitrite in the brain. In comparison, noscapine pretreatment attenuated PTZ-induced behavioural and biochemical changes in the animals. The results indicate that noscapine ameliorates the oxido-nitrosative stress. However, studies indicate that oxido-nitrosative stress is a significant concern for the GABAergic neurons and promotes the disease progression. Further studies are required to explore the molecular mechanism of noscapine, which might be a practical approach as a newer antiepileptic agent. � 2023 John Wiley & Sons Australia, Ltd. | en_US |
| dc.identifier.doi | 10.1111/1440-1681.13825 | |
| dc.identifier.issn | 3051870 | |
| dc.identifier.uri | http://10.2.3.109/handle/32116/4395 | |
| dc.identifier.url | https://onlinelibrary.wiley.com/doi/10.1111/1440-1681.13825 | |
| dc.language.iso | en_US | en_US |
| dc.publisher | John Wiley and Sons Inc | en_US |
| dc.subject | antioxidant | en_US |
| dc.subject | epilepsy | en_US |
| dc.subject | neuroprotection | en_US |
| dc.subject | noscapine | en_US |
| dc.subject | pentylenetetrazole | en_US |
| dc.title | Impact of noscapine on halting the progression of pentylenetetrazole induced kindling epilepsy in mice | en_US |
| dc.title.journal | Clinical and Experimental Pharmacology and Physiology | en_US |
| dc.type | Article | en_US |
| dc.type.accesstype | Closed Access | en_US |