ArticleIranian journal of pharmaceutical research : IJPR
Therapeutic Investigation of Zingerone Against Pentylenetetrazole-Induced Kindled Seizures in Mice.
Article in Iranian journal of pharmaceutical research : IJPR. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Epilepsy is a condition characterized by frequent bursts of neuro-electrical impulse activity in the brain, involving the expression of transient receptor potential vanilloid receptor 1 (TRPV1). Zingerone (ZO) is known to possess a multitude of regulatory mechanisms for TRP channels. However, clear evidence of ZO in the regulation of TRPV1 expression has not yet been reported. Objectives: The present study was designed to evaluate the therapeutic role of ZO against pentylenetetrazole (PTZ)-induced kindled seizures (KS) in mice. Methods: The KS were induced by intraperitoneal (i.p.) administration of three doses of PTZ (35 mg/kg/day) in mice on every alternate day (day 1, 3, and 5). Additionally, the PTZ challenge test was performed on day 20. The ZO doses of 25 and 50 mg/kg; TRPV1 antagonist, i.e., selective TRPV1 antagonist (SB-366791, 10 mg/kg); and a combination of ZO and SB-366791 were administered orally (p.o.). The seizure score was assessed using Racine's scoring system on day 20. Changes in KS-associated spatial cognition were assessed by the water Y-maze and water T-maze tests. The hippocampal tissue biomarkers, i.e., thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), tumor necrosis factor-alpha (TNF-α), and TRPV1 expression were estimated. Results: The ZO attenuates the PTZ-induced changes in Racine's scores and spatial cognition effects in Y-maze and water T-maze tests. Furthermore, ZO also ameliorates the PTZ-induced biomarker changes. Conclusions: Hence, ZO possesses therapeutic potential against KS conditions in mice via regulation of TRPV1 channel functions. However, more extensive studies are required to prove this therapeutic potency in different seizure conditions across various animal species.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.