1-Deoxynojirimycin (1-DNJ) is a naturally occurring sugar analogue with unique bioactivities. It is found in mulberry leaves and silkworms, as well as in the metabolites of certain microorganisms, including Streptomyces and Bacillus. 1-DNJ is a potent α-glucosidase inhibitor and it possesses anti-hyperglycemic, anti-obese, anti-viral and anti-tumor properties. Some derivatives of 1-DNJ, like miglitol, miglustat and migalastat, were applied clinically to treat diseases such as diabetes and lysosomal storage disorders. The present review focused on the extraction, determination, pharmacokinetics and bioactivity of 1-DNJ, as well as the clinical application of 1-DNJ derivatives.

Cerebral ischemia–reperfusion injury (CIRI) is a complex pathological process that arises when blood flow is restored to the brain after ischemia, often resulting in significant neuronal damage and triggering secondary inflammatory responses. This review explores the immune mechanisms underlying CIRI, focusing on the activation and polarization of resident central nervous system (CNS) cells—particularly microglia and astrocytes—and the infiltration of peripheral immune cells such as neutrophils, monocytes/macrophages, and T lymphocytes. We discuss the central role of microglia in the neuroinflammatory cascade, their polarization between pro-inflammatory (M1) and anti-inflammatory (M2) phenotypes, and how this process influences neuronal damage and tissue repair. This review highlights the roles of the complement system, inflammasome activation, and blood–brain barrier disruption as key drivers of inflammation and neuronal injury. Additionally, we elaborate on the dynamic interactions between resident and infiltrating immune cells, which amplify inflammation and impede post-ischemic recovery. Finally, we discuss emerging therapeutic strategies targeting immune modulation, including cytokine regulation, microglial reprogramming, and targeted drug delivery systems, which offer promising avenues for improving outcomes in ischemic stroke.

The temporary or permanent occlusion of cerebral blood vessels results in ischemic stroke (IS). Ischemia per se causes focal neuronal damage, and the subsequent ischemia–reperfusion injury that occurs after blood flow restoration further compromises brain tissue and cells in the neurovascular unit, significantly contributing to poor patient outcomes and functional impairments. Current research indicates that the ubiquitin–proteasome system (UPS) plays a crucial role in the pathological processes associated with cerebral ischemia–reperfusion injury (CIRI). Notably, E3 ubiquitin (Ub) ligases, which are essential in the UPS, have garnered increasing attention as potential novel therapeutic targets for treating ischemia–reperfusion damage in the brain. This review focuses primarily on the background of E3 Ub ligases and explores their intricate relationships with the pathological processes of CIRI.

Cerebral ischemia‐reperfusion (I/R) injury often causes significant neuronal damage, neurological deficits, and long‐term disability. This study investigates the role of tripartite motif‐protein 56 (TRIM56) in cerebral I/R injury and elucidates the underlying mechanisms. Here, a significant increase in TRIM56 expression in the human brain, mouse brain, and primary neurons after cerebral I/R injury is first detected. TRIM56 knockout mice exhibit reduced neurological deficits and a diminished inflammatory response, with TRIM56 overexpression intensifying these effects. Mechanistic investigations demonstrate that TRIM56 promotes neuronal ferroptosis by directly interacting with Krüppel‐like factor 4 (KLF4) and triggering its K48‐linked ubiquitination‐dependent degradation. Moreover, compound screening identifies farudodstat as a potential TRIM56 inhibitor to reduce I/R injury in vivo and in vitro. In conclusion, TRIM56 critically regulates neuronal damage during cerebral I/R injury, thereby presenting as a potential therapeutic target for reducing brain I/R injury. Novel therapeutic strategies inhibiting TRIM56 or its downstream signaling pathways may be developed to mitigate the devastating effects of I/R injury on neuronal survival and function.

Non-alcoholic fatty liver disease (NAFLD) is one of the most prevalent chronic liver diseases globally. Hepatic steatosis, characterized by the accumulation of lipid droplets (LDs), is a hallmark of NAFLD. Traditional pathology and specific fluorescent dye imaging have difficulty in observing LDs in their natural state within hepatocytes rapidly. In this study, a customized dynamic full-field optical coherence tomography (D-FFOCT) system was applied for label-free visualization of LDs and rapid ex vivo assessment of NAFLD. Two groups of mice fed the methionine choline-deficient (MCD) diet for one week and two weeks, respectively, underwent dual-mode FF-OCT imaging and comparative quantitative analysis. The subcellular structures—including nuclei and small LDs—were clearly observed. Quantitative analysis of D-FFOCT results revealed significant quantitative profiles in LD characteristics across various NAFLD stages. Furthermore, imaging of a non-alcoholic steatohepatitis (NASH) mouse model fed a high-fat diet for 14 weeks provided insights into the identification of inflammatory cells via D-FFOCT. These results indicate that D-FFOCT can effectively resolve the subcellular structure and quantify LDs in NAFLD models across varying severities, thereby demonstrating its potential for rapid NAFLD assessment and pharmaceutical development applications.

Ischemic stroke, induced by the occlusion of cerebral blood vessels, represents a leading cause of global morbidity and mortality. Although thrombolytic therapy and mechanical thrombectomy are cornerstone treatments for restoring cerebral perfusion, their clinical effectiveness is severely constrained by a narrow therapeutic window. This study presents a reactive oxygen species (ROS) - responsive hydrogel platform loaded with engineered apoptotic vesicles (apoVs) designed to simultaneously target multiple post-stroke pathological processes. Proteomic analyses reveal that apoV isolated from apoptotic neural stem cells are enriched in proteins associated with angiogenesis and neuroprotection. In vitro investigations and in vivo animal experiment further demonstrate that the hydrogel can alleviate oxidative stress, promote angiogenesis and protect nerve injury by releasing hydrogen sulfide (H₂S) - functionalized apoV in the infarct area. In summary, this hydrogel platform holds considerable therapeutic promise by transforming the hostile post-stroke microenvironment into a regeneration-permissive niche, thereby fostering endogenous tissue repair.