ArticlePhysiological research2022
Ellagic acid attenuates muscle atrophy in STZ-induced diabetic mice.
Article in Physiological research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- Ellagic acid as potential therapeutic compound for diabetes and its complications: a systematic review from bench to bed.Naunyn-Schmiedeberg's archives of pharmacology · 2024Pooled it
- Chestnut (Nutrients · 2025Article
- Effects of Ellagic Acid and Berberine on Hind Limb Ischemia Reperfusion Injury: Pathways of Apoptosis, Pyroptosis, and Oxidative Stress.Medicina (Kaunas, Lithuania) · 2025Article
- Review
- The Effects of Ellagic Acid on Experimental Corrosive Esophageal Burn Injury.Current issues in molecular biology · 2024Article
- Activation of Lactate Receptor Positively Regulates Skeletal Muscle Mass in Mice.Physiological research · 2023Article
- The impact of heat therapy on neuromuscular function and muscle atrophy in diabetic rats.Frontiers in physiology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetes is closely connected with skeletal muscle dysfunction. Ellagic acid (EA) possesses a variety of bio-effects and is applied to the improvement of diabetes. The purpose of this study was to explore the potential improvement effect and mechanisms of EA in streptozotocin (STZ)-induced diabetic muscle atrophy. The model of diabetic mice was established by intra-peritoneal STZ to evaluate treatment effect of EA (100 mg/kg/d for 8 weeks) on muscle atrophy. Our data exhibited that EA enhanced fiber size and weight of gastrocnemius, and promoted grip strength to relieve STZ-induced muscle lesions. In serum, the levels of Creatine kinase (CK), lactate dehydrogenase (LDH), total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL) were inhibited, while high-density lipoprotein cholesterol (HDL) level was enhanced by EA treatment in diabetic mice. In gastrocnemius, EA decreased Atrogin-1 and MuRF-1 expressions to relieve STZ-induced muscle atrophy. Moreover, EA increased NRF-1 and PGC-1alpha expressions to alleviate mitochondrial disorder. Meanwhile, EA suppressed CHOP and GRP-87 levels to relieve ER stress. Lastly, EA inhibited BAX expressions and enhanced Bcl-2 expressions to mitigate apoptosis. In conclusion, EA is preventing the event of STZ-induced gastrocnemia by amelioration of mitochondrial dysfunction, ER stress and apoptosis, and could be used in the protection and therapeutic of muscle atrophy in diabetes.
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