ArticleJournal of inflammation research2025
Volatile Oil From
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- The dual role of endoplasmic reticulum stress in cerebral ischemia: from adaptive protection to apoptotic induction.Frontiers in molecular neuroscience · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: To investigate the synergistic protective effects and underlying mechanisms of combining Patients and Methods: An MIRI model was established in Sprague-Dawley rats to evaluate the synergistic cardioprotective effects of VOA combined with Cre. Myocardial injury was assessed by measuring the infarct size, apoptotic cardiomyocytes, myocardial injury biomarkers, and histopathological changes. Proinflammatory mediators and oxidative stress markers and results of Western blotting were analyzed to determine the underlying cardioprotective mechanisms of Cre and VOA. In addition, metabolomic analysis was conducted to identify alterations in relevant metabolic pathways. Results: Cre and VOA alleviated MIRI in rats by reducing infarct size, lowering the levels of myocardial injury biomarkers (Lactate dehydrogenase (LDH), cardiac troponin I (cTnI), creatine kinase (CK), and creatine kinase-myocardial band (CK-MB)), and ameliorating histopathological damage. Mechanistically, Cre and VOA attenuated oxidative stress by enhancing the activity of the antioxidant enzyme superoxide dismutase (SOD) and suppressing the expression of the oxidative stress marker malondialdehyde (MDA). In addition, they downregulated proinflammatory cytokines (interleukin-6 (IL-6) and interleukin-1β (IL-1β)) by inhibiting the MAPK/NF-κB/TNF-α signaling pathway. They mitigated endoplasmic reticulum (ER) stress and apoptosis by modulating the GRP78-PERK/ATF6-CHOP pathway. Metabolomic analysis identified 13 potential biomarkers, and glutamic, pantothenic, and oleic acids were the key metabolites. The glycine, serine, and threonine metabolism pathway, glutathione metabolism, the pentose phosphate pathway, and the biosynthesis of unsaturated fatty acids were the most relevant metabolic pathways involved in the cardioprotective effects of Cre and VOA. Conclusion: Cre and VOA may alleviate MIRI by modulating energy metabolism and suppressing apoptosis and inflammatory responses triggered by oxidative and ER stress. This effect is mediated by GRP78-PERK/ATF6-CHOP and MAPK-NF-κB-TNF-α signaling pathways. Moreover, the volatile oil of
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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.