Electroacupuncture pre-treatment exerts a protective effect on LPS-induced cardiomyopathy in mice through the delivery of miR-381 via exosomes.

OBJECTIVE: This study aims to investigate the cardiac protective effects and molecular mechanisms of electroacupuncture (EA) pre-treatment in lipopolysaccharide (LPS)-Induced Cardiomyopathy. METHODS AND RESULTS: Pre-treatment with EA was performed 30 min before intraperitoneal injection of LPS. Cardiac function changes in mice of the EA + LPS group were observed using electrocardiography, echocardiography, and enzyme linked immunosorbent assay (ELISA) and compared with the LPS group. The results demonstrated that EA pre-treatment significantly improved the survival rate of septic mice, alleviated the severity of endotoxemia, and exhibited notable cardiac protective effects. These effects were characterized by a reduction in ST-segment elevation on electrocardiography, an increase in ejection fraction (EF) and fraction shortening (FS) on echocardiography and a decrease in the expression of serum cardiac troponin I (cTn-I) levels. Serum exosomes obtained after EA pre-treatment were extracted and administered to septic mice, revealing significant cardiac protective effects of EA-derived exosomes. Furthermore, the antagonism of circulating exosomes in mice markedly suppressed the cardiac protective effects conferred by EA pre-treatment. Analysis of serum exosomes using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) revealed a significant upregulation of miR-381 expression after EA pre-treatment. Inhibition or overexpression of miR-381 through serotype 9 adeno-associated virus (AAV9)-mediated gene delivery demonstrated that overexpression of miR-381 exerted a cardiac protective effect, while inhibition of miR-381 significantly attenuated the cardiac protective effects conferred by EA pre-treatment. CONCLUSIONS: Our research findings have revealed a novel endogenous cardiac protection mechanism, wherein circulating exosomes derived from EA pre-treatment mitigate LPS-induced cardiac dysfunction via miR-381.

In-situ synthesis of ZIF-8 on magnetic pineapple leaf biochar as an efficient and reusable adsorbent for methylene blue removal from wastewater.

The presence of organic dyes in aquatic systems poses a significant threat to ecosystems and human well-being. Due to recycling challenges, traditional commercial activated carbon is not cost-effective. To address this, an imidazolate acid zeolite framework-8 (ZIF-8)-modified magnetic adsorbent (ZMPLB-800) was synthesized through the in-situ formation of ZIF-8 and subsequent carbonization at 800 °C, using magnetic pineapple leaf biochar (MPLB) as a carrier. The porous structure of ZMPLB-800 facilitates the rapid passage of dye molecules, enhancing adsorption performance. ZMPLB-800 exhibited remarkable adsorption capacity for methylene blue (MB) across a pH range of 3-13, with a maximum adsorption capacity of 455.98 mg g-1. Adsorption kinetics and thermodynamics followed the pseudo-second-order kinetic model and Langmuir isotherm model. Mechanisms of MB adsorption included pore filling, hydrogen bonding, electrostatic interactions, π-π interactions, and complexation through surface functional groups. Additionally, ZMPLB-800 demonstrated excellent regeneration performance, recording a removal efficiency exceeding 87% even after five adsorption/desorption cycles. This study provides a novel strategy for treating dye wastewater with MOF composites, laying the foundation for waste biomass utilization.

The role of the peripheral system dysfunction in the pathogenesis of sepsis-associated encephalopathy.

Sepsis is a condition that greatly impacts the brain, leading to neurological dysfunction and heightened mortality rates, making it one of the primary organs affected. Injury to the central nervous system can be attributed to dysfunction of various organs throughout the entire body and imbalances within the peripheral immune system. Furthermore, central nervous system injury can create a vicious circle with infection-induced peripheral immune disorders. We collate the pathogenesis of septic encephalopathy, which involves microglial activation, programmed cell death, mitochondrial dysfunction, endoplasmic reticulum stress, neurotransmitter imbalance, and blood-brain barrier disruption. We also spotlight the effects of intestinal flora and its metabolites, enterocyte-derived exosomes, cholinergic anti-inflammatory pathway, peripheral T cells and their cytokines on septic encephalopathy.