ArticleChemistryOpen2026
Epoxy Clerodane Diterpene Attenuates the Differentiated Adipocyte Hypertrophy and Enhances Mitochondrial Metabolism.
Article in ChemistryOpen, 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
5 authors.
Funding
Abstract
Adipocyte hypertrophy is an obesity-related metabolic dysfunction, which is frequently associated with decreased mitochondrial activity during adipocyte development. The current study aimed to assess the potential of epoxy clerodane diterpene (ECD) (IUPAC: 5R, 10R)-4R, 8R-dihydroxy-2S, 3R:15, 16-diepoxycleroda-13(16), 17, 12S:18,1S-dilactone) extracted from Cassia tora on adipocyte differentiation, lipid accumulation, mitochondrial function, and inflammation. Human bone marrow mesenchymal stem cells (hMSCs) were stimulated into adipocytes using the standard differentiation medium. The methodological design included the evaluation of ECD cytotoxicity, lipid accumulation, mitochondrial membrane potential, qRT-PCR, and ELISA. ECD didn't significantly reduce the cellular viability; however, it decreased lipid accumulation by 65%, 87%, and 87.5% at doses of 2, 4, and 8 μM, respectively. Also, at 4 µM of ECD, it decreased adipocyte hypertrophy, increased mitochondrial membrane potential, raised the expression of thermogenesis-related genes (UCP-1, PPARγC1α, SREBP1c), decreased the expression of adipogenic proteins (C/EBPα, PPARγ), increased adiponectin levels, and reduced inflammatory markers (IL-4, TNF-α) compared to untreated controls. Thus, ECD may hold tremendous promise as a natural agent for controlling adipogenesis, and its impacts on lipid metabolism, mitochondrial function, and inflammatory responses demonstrate its potential for therapeutic use in the treatment of obesity and associated metabolic diseases.
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.