ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Lower L-glutamine abundance and higher HSPA8 activity contribute to the mitigation of ethanol-induced liver cell injury by thymol.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. 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
9 authors.
Funding
Abstract
Ethanol metabolism activates the generation of reward value by neurons, but it results in liver injury. The underlying processes through which thymol mitigates liver injury caused by ethanol exposure remain incompletely understood. In the present study, thymol alleviated ethanol-induced a decrease in superoxide dismutase activity. Thymol attenuated ethanol-induced elevation of lipid accumulation, as evidenced by a lesser number of larger lipid droplets and lower lipid synthesis. Correspondingly, thymol was found to counteract ethanol-induced downregulation in the ratio of phospho-AMPKα to total AMPKα. Altered metabolites in cells treated with ethanol plus thymol were notably enriched in purine metabolism, citric acid cycle, mitochondrial electron transport chain, and glycerol phosphate shuffle. Thymol inhibited ethanol-induced elevation in L-glutamine abundance. Further investigations revealed that supplementation with L-glutamine intensified the damage induced by ethanol. This exacerbation was manifested through increased levels of total cholesterol and triglyceride, a greater number of larger lipid droplets, and reduced superoxide dismutase activity. Moreover, we found that the improving effect of thymol on ethanol-induced autophagic flux obstruction was mediated by higher abundances of glycosylated LAMP1 and ATP6V1B2 proteins. Finally, VER-155008, an inhibitor of heat shock protein 8, abolished the effects of thymol on ethanol-induced increases in the abundances of Il6 mRNA, Tnf mRNA, Tgfb1 mRNA, malondialdehyde, Fasn mRNA, Srebf1 mRNA, and Xdh mRNA, the LC3-II/LC3-I ratio, and SQSTM1 protein. VER-155008 also blocked the effect of thymol on ethanol-induced a reduction in glycosylated LAMP1 protein expression. These data provide novel insights into the impact of thymol on ethanol-induced liver injury.
Indexed as
Identifiers
41134352What 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.