ArticleDrug design, development and therapy2026
In-vivo Antioxidant Effects of Emodin on Ischemia-Reperfusion Injury of Rat's Skeletal Muscle.
Article in Drug design, development and therapy, 2026. 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.
- Emodin in Skeletal Muscle Ischemia-Reperfusion: Model Validity and Analytical Concerns [Letter].Drug design, development and therapy · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Skeletal muscle ischemia-reperfusion (I/R) injury is a clinically significant condition characterized by oxidative stress, inflammation, and histological damage. Emodin, a natural anthraquinone derivative, has been shown to exert antioxidative, anti-inflammatory, and antiapoptotic effects in various organ systems, however its efficacy in skeletal muscle I/R injury remains unclear. This study aimed to evaluate the potential protective role of emodin in a rat model of skeletal muscle I/R injury using biochemical and histopathological assessments. Methods: Twenty-four male Wistar rats were randomly assigned to four groups: Sham (S), Emodin (E) (20 mg/kg intraperitoneal), Ischemia-Reperfusion (IR), and IR with E treatment (IR+E). Skeletal muscle I/R was induced by infrarenal aortic clamping for 45 minutes, followed by 120 minutes of reperfusion. Muscle tissue was analyzed for malondialdehyde (MDA) and glutathione (GSH) levels, as well as catalase (CAT) and superoxide dismutase (SOD) activities. Histopathological evaluation included semiquantitative scoring of muscle fiber disorganization, neutrophil infiltration, interstitial edema, and hemorrhage. Results: The IR group demonstrated significantly elevated MDA levels and decreased CAT activity compared with controls. E treatment markedly reduced MDA levels and partially restored CAT activity, while no significant changes were observed in SOD or GSH. Histopathological analysis showed severe disorganization, neutrophil infiltration, and edema in the IR group, which were notably attenuated by emodin, though not completely prevented. Conclusion: Emodin confers partial protection against skeletal muscle I/R injury, primarily by inhibiting lipid peroxidation and partially restoring CAT activity. This study provides the first in-vivo evidence of emodin's effects in skeletal muscle I/R, highlighting its potential as a tissue-specific antioxidant intervention and warranting further investigation of its mechanistic pathways.
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.