Photodynamic therapy of severe hemorrhagic shock on yolk–shell MoS2 nanoreactors

Abstract

Ischemia-reperfusion injury resulting from severe hemorrhagic shock continues to cause substantial damage to human health and impose a significant economic burden. In this study, we designed an Au-loaded yolk–shell MoS₂ nanoreactor (Au@MoS₂) that regulates cellular homeostasis. In vitro experiments validated the efficacy of the nanomaterial in reducing intracellular reactive oxygen species (ROS) production during hypoxia and reoxygenation, and had great cell biocompatibility, Au@MoS₂. The antioxidant properties of the nanoreactors contributed to the elimination of ROS (over twofold scavenging ratio for ROS). In vivo results demonstrate that Au@MoS₂ (54.88% of reduction) alleviates hyperlactatemia and reduces ischemia-reperfusion injury in rats subjected to severe hemorrhagic shock, compared to MoS₂ (26.32% of reduction) alone. In addition, no discernible toxic side effects were observed in the rats throughout the experiment, underscoring the considerable promise of the nanoreactor for clinical trials. The mechanism involves catalyzing the degradation of endogenous lactic acid on the Au@MoS₂ nanoreactor under 808 nm light, thereby alleviating ischemia-reperfusion injury. This work proposes a new selective strategy for the treatment of synergistic hemorrhagic shock.