abinScience May 2026 Literature Digest: Stroke Nanoplatforms, African Swine Fever Autophagy Evasion & Post-Sepsis Cognitive Impairment

Cerebral ischemia-reperfusion injury (CIRI) following recanalization in acute ischemic stroke (AIS) remains a major driver of neuronal death. Its pathological mechanisms involve a cascading amplification of oxidative stress and neuroinflammation, while conventional drug delivery systems struggle to effectively cross the blood-brain barrier (BBB) and simultaneously modulate multiple pathological pathways. To address this challenge, the study adopted an integrative philosophy combining traditional herbal medicine with Western pharmacology, co-assembling baicalein (BLN)—a natural flavonoid derived from Scutellaria baicalensis—with rapamycin (RAP) into carrier-free binary nanoparticles (BR NPs) via self-assembly. These were further functionalized with DSPE-PEG₂ₖ-Angiopep-2 to yield targeted ABR NPs. The resulting nanoplatform achieved a total drug loading of approximately 77.01% with excellent colloidal stability, enabling efficient BBB penetration and neuronal targeting via LRP1 receptor-mediated endocytosis. In vitro studies demonstrated that ABR NPs possessed broad-spectrum, potent ROS-scavenging activity and markedly promoted microglial polarization from the pro-inflammatory M1 phenotype toward the anti-inflammatory M2 phenotype. In a mouse MCAO model, ABR NPs reduced infarct volume from 37.88% to just 7.84%, significantly outperforming individual drug treatments and non-targeted controls, while effectively suppressing neuronal apoptosis and reducing pro-inflammatory cytokine levels. These findings establish that ABR NPs achieve precise brain-targeted therapy through a dual-pathway synergistic mechanism (ROS scavenging + neuroinflammation suppression), offering a promising new avenue for the clinical translation of CIRI treatment.

African swine fever (ASF) is a highly lethal infectious disease caused by African swine fever virus (ASFV), for which no effective vaccine or treatment currently exists. Autophagy is an important host defense mechanism against pathogens, yet viruses frequently hijack it to facilitate their own replication. The specific molecular mechanisms by which ASFV evades autophagy, however, remain poorly understood. This study focused on the I10L protein encoded within the right variable region of the ASFV genome, revealing that it markedly suppresses autophagic flux and leads to extensive autophagosome accumulation. Mechanistically, I10L localizes to late endosomal/lysosomal membranes and directly binds RAB7, competitively blocking the assembly of the RAB7-HOPS complex and thereby impairing the SNARE complex assembly required for autophagosome-lysosome fusion, ultimately preventing autolysosome formation. Deletion of I10L substantially attenuated viral replication and restored autophagic flux. Collectively, this study uncovers an immune evasion strategy in which ASFV exploits I10L to manipulate the RAB7-HOPS axis and escape lysosomal degradation, providing new insights for antiviral target development.

Post-sepsis cognitive impairment (PSCI) is a major challenge in critical care medicine, manifesting as persistent memory deficits, attention impairment, and executive dysfunction in sepsis survivors, with no effective clinical interventions currently available. Lactate, a glycolytic end product traditionally regarded as a marker of poor prognosis, has more recently been recognized as serving a dual role as both an energy substrate and a signaling molecule. This study employed cecal ligation and puncture (CLP) to establish a mouse model of PSCI and investigated the neuroprotective effects and underlying mechanisms of exogenous lactate supplementation. Lactate treatment significantly improved survival rates and body weight recovery in septic mice, as well as cognitive performance across multiple behavioral assessments. At the molecular level, lactate suppressed the HMGB1/RAGE signaling axis, reduced neuronal apoptosis, lowered levels of brain injury biomarkers, attenuated excessive glial activation, modulated the neuroinflammatory microenvironment, and alleviated oxidative stress. In addition, lactate upregulated the expression of multiple neurotransmitter receptors, suggesting a restorative effect on synaptic plasticity. Taken together, lactate demonstrates significant neuroprotective potential against PSCI by improving cerebral energy metabolism, suppressing neuroinflammation, and reducing oxidative stress.