Magnesium hydride attenuates intestinal barrier injury during hemorrhage shock by regulating neutrophil extracellular trap formation via the ROS/MAPK/PAD4 pathway.

Magnesium hydride (MgH2) is a hydrogen storage material that is known for its high capacity and safety and is capable of releasing hydrogen in a controlled manner when administered orally. This release of hydrogen has been associated with a range of biological effects, including anti-inflammatory properties, antioxidant activity, and protection of the intestinal barrier. Previous research has shown that neutrophil extracellular traps (NETs) play a role in the dysfunction of the intestinal barrier in conditions such as sepsis and critical illnesses. However, it remains unclear as to whether MgH2 can protect the intestinal barrier by inhibiting NET formation, and the underlying mechanisms have yet to be elucidated. A rat model of hemorrhagic shock was created, and pretreatment or posttreatment procedures with MgH2 were performed. After 24 h, samples from the small intestine and blood were collected for analysis. In vitro, human neutrophils were incubated with either phorbol-12-myristate-13-acetate (PMA) or MgH2. Reactive oxygen species generation and the expression of key proteins were assessed. The results demonstrated that MgH2 administration led to a decrease in inflammatory cytokines in the serum and mitigated distant organ dysfunction in rats with HS. Furthermore, MgH2 treatment reversed histopathological damage in the intestines, improved intestinal permeability, and enhanced the expression of tight junction proteins (TJPs) during HS. Additionally, MgH2 treatment was found to suppress NET formation in the intestines. In vitro pretreatment with MgH2 alleviated intestinal monolayer barrier disruption that was induced by NETs. Mechanistically, MgH2 pretreatment reduced ROS production and NET formation, inhibited the activation of ERK and p38, and suppressed the expression of the PAD4 protein. These findings indicated that MgH2 may inhibit NET formation in a ROS/MAPK/PAD4-dependent manner, which reduces NET-related intestinal barrier damage, thus offering a novel protective role in preventing intestinal barrier dysfunction during HS.

MXene-enhanced ePatch with antibacterial activity for wound healing.

Prudent wound-healing strategies hold great potential in expediting tissue renovation and regeneration. Despite the widespread adoption of hydrogels as preferred carriers for wound healing patches, achieving optimal mechanical compatibility and superior wound performance remains a formidable challenge. Consequently, meticulous attention must be given to the formulation of hydrogel structure and materials design to overcome these hurdles. In response, we have developed an ePatch composed of polyacrylamide (PAAM) as the primary hydrogel structure, augmented with MXene, silver nanowires (AgNWs), and resveratrol to act as sustained-release agents, structural enhancers, and antibacterial agents, respectively. Notably, the ePatch exhibited exceptional wound-fitting capabilities and impressive mechanical stretchability (with a relative standard deviation [RSD] of only 1.36% after 55 stretches) and Young's modulus. In contrast to the commercial 3M Tegaderm, the ePatch demonstrated superior wound healing properties, with the inclusion of MXene into PAAM/AgNWs playing a pivotal role in expanding the ePatch's potential use across various interconnected fields.

Melatonin protects against myocardial ischemia-reperfusion injury by elevating Sirtuin3 expression and manganese superoxide dismutase activity.

Myocardial ischemia-reperfusion (MI/R) injury is a crucial cause for mortality throughout the world. Recent studies indicated that melatonin might exert profound cardio-protective effect in MI/R injury. However, the underlying mechanisms are not completely understood. In the current study, we aimed to explore the potential effect of melatonin in the pathological process of MI/R. Both in vivo MI/R model and in vitro H9c2 cell line simulated I/R (SIR) model were applied with or without melatonin supplementation. We found that Sirtuin3 (Sirt3) expression and activity were markedly decreased under MI/R and SIR conditions. Melatonin treatment significantly increased myocardial Sirt3 expression, and alleviated MI/R-induced cardiac morphology changes and cardiac dysfunction, as well as myocardial apoptosis level. In addition, DHE and JC-1 staining results demonstrated that melatonin reduced mitochondrial reactive oxygen species (ROS) generation and restored ATP production after SIR injury via elevating Sirt3 expression. By using siRNA targeting Sirt3, we confirmed that the beneficial effects of melatonin were dependent on Sirt3, which in turn deacetylated and activated manganese superoxide dismutase (MnSOD). Collectively, the current study demonstrated the protective effect of melatonin against MI/R injury via alleviating myocardial oxidative stress. Moreover, these beneficial effects were associated with the deacetylation modification of Sirt3 on MnSOD.

Aortic Dissection Presenting as Septic Shock: A Case Report and Literature Review.

Acute aortic dissection is a life-threatening clinical emergency, which mostly occurs in aged patients and presents with sharp chest pain. In this paper, we reported a case of acute aortic dissection, which induced septic shock in a young woman, without typical chest pain. The septic shock was possibly due to the bacterial translocation caused by aortic dissection-induced intestinal ischemia and intestinal epithelial barrier dysfunction. Our case appeared as the first case report of aortic dissection presenting as septic shock. This case is rare but can serve as a reminder that aortic dissection may be accompanied by septic shock, and this could result in a grave outcome.