ArticleScientific reports2024
Exploration of neuroprotective effect from Coriandrum sativum L. ethanolic seeds extracts on brain of obese rats.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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
4 citing papers in PubMed, 7 citations in OpenAlex.
- Regulatory impact of intermittent fasting on autophagy in high fat diet induced structural and cognitive brain deteriorations in rats.Scientific reports · 2026Article
- Review
- Licochalcone A prevents cognitive decline in a lipopolysaccharide-induced neuroinflammation mice model.Molecular medicine (Cambridge, Mass.) · 2025Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
In this study, the potential neuroprotective ability of coriander seeds (Coriandrum sativum L.) ethanolic extract (CSES) as a neuroprotectant agent in the brains of high-fat diet-induced obese rats was analyzed. The study investigated how CSES impacts oxidative stress markers (i.e., malondialdehyde/MDA, glutathione/GSH and catalase), inflammation marker (i.e., Interleukin-6/IL-6), cellular senescence markers (i.e., senescence-associated β-galactoside/SA-β-Gal activity and p16), brain damage marker (i.e., Neuron-specific Enolase/NSE), and neurogenesis markers (i.e., mature Brain-derived Neurotropic Factor/BDNF, pro-BDNF, and mature/pro-BDNF ratio). Male adult Wistar rats were fed a high-fat diet and given CSES once daily, at 100 mg/kg body weight, for 12 weeks. CSES significantly reduced MDA concentration (p = < 0.001), SA-β-Gal activity (p = 0.010), and increased GSH concentration (p = 0.047) in the brain of obese rats; however, the decrease of IL-6, NSE, and p16 as well as the increase of catalase specific activity and BDNF expression were not significant. Moreover, the mature/pro-BDNF ratio was significantly higher in the brains of non-obese rats, both given the control diet and the high-fat diet compared to the control. Our results suggest that obese rats benefited from consuming CSES, showing improved oxidative stress levels, reduced cellular senescence and increased endogenous antioxidants, making CSES a potential neuroprotective agent.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.