Lycium barbarum polysaccharides loaded myocardial-decorating nanoplatform for precise treatment of myocardial injury induced by exertional heat stroke
- Int J Biol Macromol. 2026 Apr:354:151468. doi: 10.1016/j.ijbiomac.2026.151468.
- 1. School of Public Health, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, 750004, PR China.
- 2. State Key Laboratory of Chinese Medicine Modernization, Tianjin University of Traditional Chinese Medicine, Jinghai, Tianjin, 301617, PR China.
- 3. School of Public Health, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, 750004, PR China; School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, 750004, PR China.
- 4. Hospital of Ningxia Hui Autonomous Region, Yinchuan, Ningxia Hui Autonomous Region, 750004, PR China.
- 5. School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, 750004, PR China. Electronic address: [email protected].
- 6. School of Public Health, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, 750004, PR China; School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, 750004, PR China. Electronic address: [email protected].
Exertional heat stroke (EHS) presents a significant public health risk, with recent studies highlighting the role of arachidonic acid 15-lipoxygenase-1 (ALOX15)-mediated Ferroptosis in EHS-induced cardiac damage. Although Lycium barbarum Polysaccharides (LBP) have shown potential in treating heart diseases, their effectiveness is limited by poor targeting and low bioavailability. Herein, we delicately engineered a myocardial-targeted lycium barbarum polysaccharide-loaded nanoparticle (PCM/LBP@MPDA) for EHS myocardial injury treatment. PCM/LBP@MPDA achieves precise myocardial targeting through the PCM (WLSEAGPVVTVRALRGTGSW) and subsequently inhibits Ferroptosis by scavenging Reactive Oxygen Species and chelating iron. Upon immediate cellular uptake of PCM/LBP@MPDA by cardiomyocytes, MPDA could can chelate with iron ions and elininate Reactive Oxygen Species, while the released LBP was capable of supressing Ferroptosis by downregulating ALOX15 and upregulating Glutathione Peroxidase 4, thereby contributing to an effective decay of the cardiomyocytes Ferroptosis and management of the cardiac function in EHS mice via suppressing oxidative stress and Ferroptosis. Overall, our findings pave a broad avenue for precise myocardial injury treatment, and point out a promising direction for clinical translation.
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