ArticleOpen life sciences2025
Maslinic acid improves mitochondrial function and inhibits oxidative stress and autophagy in human gastric smooth muscle cells.
Article in Open life sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Food and Medicine Homology Substances as Potential Modulators of the Gut-Muscle Axis in Animal Meat Quality: A Review.Foods (Basel, Switzerland) · 2026Review
- Role of maslinic acid in ischemia-reperfusion-induced testicular injury in rats.Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES · 2026Article
- SIRT1-mediated deacetylation of DRP1 suppresses excessive mitophagy and ameliorates pediatric functional dyspepsia.BMC immunology · 2026Article
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Authors and funding
3 authors.
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Abstract
Functional dyspepsia (FD) is a chronic disease that occurs in the gastroduodenal region and significantly impacts human health. Maslinic acid (MA), a pentacyclic triterpene acid, is the primary bioactive ingredient in Chinese medicinal herbs such as hawthorn, which exhibits beneficial impacts on the regulation of various disease progressions. However, the specific functions and associated pathways of MA in FD progression remain unclear and require further investigation. In this work, it was demonstrated that MA enhanced the cell viability of human gastric smooth muscle cells (HGSMCs). In addition, the mitochondrial dysfunctions induced by carbonyl cyanide 3-chlorophenylhydrazone (CCCP) were rescued after MA treatment. Furthermore, autophagy was increased following CCCP treatment, but this phenomenon was counteracted after MA treatment. The oxidative stress, elevated after CCCP treatment, was alleviated following MA addition. Finally, the AMPK/SIRT1 pathway was suppressed after CCCP stimulation but was re-activated after MA treatment. In conclusion, it was uncovered that MA accelerated HGSMC viability and improved mitochondrial function, inhibited autophagy, alleviated oxidative stress, and stimulated the AMPK/SIRT1 pathway. This discovery may offer new insight into the therapeutic effects of MA in FD progression.
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