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Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
Published on: January 10, 2025
Dioscin ameliorates intestinal ischemia/reperfusion injury via adjusting miR-351-5p/MAPK13-mediated inflammation and
Lingli Zheng1, Xu Han2, Yupeng Hu2
1The First Affiliated Hospital of Dalian Medical University, Dalian 116011, China; College of Pharmacy, Dalian Medical University, 9 Western Lvshun South Road, Dalian 116044, China.
Abstract:
Inflammatory reaction and cell apoptosis are two important processes in intestinal ischemia/reperfusion (II/R) injury, and exploration of effective lead compounds against II/R injury via regulating inflammation and apoptosis is critical important. In this paper, the results indicated that dioscin significantly increased cell viability, and inhibited inflammation and apoptosis caused by hypoxia-reoxygenation (H/R) injury in IEC-6 cells. in vivo II/R injury, dioscin markedly suppressed inflamma- tion and apoptosis, improved pathological changes, and depressed chiu' score in rats. Mechanistic studies indicated that dioscin notably up-regulated the expression level of MAPK13 through decreasing miR-351-5p level, and thereby decreased the expression levels of p-PKD1, NF-κB, Apaf-1, cleaved Caspase-3 and cleaved Caspase-9. Furthermore, miR-351-5p mimic and inhibitor experiments in IEC-6 cells further proved that dioscin up-regulated MAPK13 expression by decreasing miR-351-5p level to inhibit inflammation and apoptosis. Therefore, dioscin showed protective effect against II/R injury via adjusting miR-351-5/MAPK13-mediated inflammation and apoptosis. Dioscin should be considered as one potent candidate and miR-351-5/ MAPK13 should be one effective drug target for the treatment of II/R injury.
Insights
Dioscin protects against intestinal ischemia/reperfusion (II/R) injury by reducing inflammation and apoptosis. It targets the miR-351-5p/MAPK13 pathway, offering a potential therapeutic strategy for II/R injury.
Area of Science:
- Gastroenterology
- Cell Biology
- Pharmacology
Background:
- Intestinal ischemia/reperfusion (II/R) injury involves significant inflammatory responses and cell apoptosis.
- Effective treatments regulating these processes are crucial for managing II/R injury.
Purpose of the Study:
- To investigate the protective effects of dioscin against II/R injury.
- To elucidate the underlying molecular mechanisms involving miR-351-5p and MAPK13.
Main Methods:
- In vitro studies using IEC-6 cells subjected to hypoxia-reoxygenation (H/R) injury.
- In vivo studies involving II/R injury models in rats.
- Mechanistic investigations including gene expression analysis and miRNA mimic/inhibitor experiments.
Main Results:
- Dioscin enhanced cell viability and inhibited H/R-induced inflammation and apoptosis in IEC-6 cells.
- In vivo, dioscin reduced inflammation, apoptosis, and improved pathological damage in rats.
- Dioscin upregulated MAPK13 by downregulating miR-351-5p, subsequently inhibiting inflammatory and apoptotic pathways.
Conclusions:
- Dioscin demonstrates significant protective effects against II/R injury.
- The therapeutic action of dioscin is mediated through the miR-351-5p/MAPK13 pathway, highlighting its potential as a drug candidate and target for II/R treatment.
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