Shizhe Li

Spinal cord injury (SCI) often leads to permanent neurological deficits, with no effective treatment currently available. Galangin is a naturally occurring flavonoid with anti‐inflammatory and antiapoptotic activities; nevertheless, its efficacy, and molecular mechanisms in SCI remain unelucidated. First, network pharmacology and Gene Expression Omnibus database analyses were used to predict target molecules and galangin signaling pathways. In vitro, LPS‐induced immortalized murine microglial (BV‐2) and rat pheochromocytoma (PC12) cells co‐cultured with conditioned medium were used to elucidate the mechanism via western blotting, immunofluorescence, qRT‐PCR, ELISA, flow cytometry, cellular thermal shift assay (CETSA), drug affinity responsive target stability (DARTS), surface plasmon resonance (SPR), and pathway agonist/inhibitor/siRNA rescue assays. In vivo, SCI rat models were established to validate the protective efficacy through behavioral, histological, and western blot analyses. Galangin alleviated pro‐inflammatory polarization and neuroinflammation in BV‐2 microglia through inhibiting the PI3K/AKT pathway. It also diminished neuronal apoptosis and enhanced axonal growth‐associated markers expression in PC12 neurons by inhibiting the JAK2/STAT1 pathway. These mechanisms were further supported experimentally using pathway agonists, inhibitors, and gene knockdown. In rats, galangin improved motor function and reduced neuroinflammation and neuronal damage. In conclusion, galangin simultaneously inhibited both pathways to alleviate neuroinflammation, decrease neuronal damage, and upregulate axonal growth‐associated markers, thereby improving neurological function in SCI. Thus, galangin is a potential protective candidate for SCI.

Spinal cord injury (SCI) is a severe condition affecting the central nervous system that often leads to varying degrees of motor and sensory impairment. Acute primary SCI is often managed with early surgical intervention; however, secondary SCI generally has a poor prognosis owing to the lack of effective drug therapy, complex pathophysiological processes, and inherent challenges of neural repair. Ferroptosis, a novel form of programmed cell death, is characterised by oxidative damage resulting from iron‐mediated accumulation of reactive oxygen species (ROS) and lipid peroxidation (LPO) within cells. This type of cell death is prevalent in various pathological processes. Although research on ferroptosis in SCI is still emerging, some inhibitors (such as target proteins and natural compounds) have shown promising results in preclinical studies. Targeting ferroptosis may be a potential strategy for treating SCI. This paper reviews the current state of research on ferroptosis in SCI by analysing recent literature and proposes future research directions, aiming to provide new insights into SCI treatment.

The current treatment regimen for spinal cord injury (SCI), a neurological disorder with a high incidence of disability, is based on early surgical decompression and administration of pharmacological agents. However, the efficacy of such an approach remains limited, and most patients have sensory and functional deficits below the level of injury, which seriously affects their quality of life. This necessitates further exploration into effective treatment modalities. In recent years, considerable advancements have been made in developing and utilizing brain–computer interfaces (BCI), which facilitate neurorehabilitation and enhance motor function by transforming brain signals into diverse forms of output commands. BCI‐assisted systems provide alternative means of rehabilitative exercise or limb movement in patients with SCI, including electrical stimulation and exoskeleton robots. BCI shows great potential in the rehabilitation of patients with SCI. This review summarizes the current research status and limitations of BCI for SCI to provide novel insights into the concept of multimodal rehabilitation and treatment of SCI and facilitate BCI's future development.

Spinal cord injury (SCI) is a serious neurological disease with an extremely high disability rate. Most patients show a loss of motor and sensory functions below the level of injury. Current treatment protocols are based on early surgical decompression and pharmacotherapy. However, the efficacy of these interventions is suboptimal. Due to its complex pathophysiological mechanisms and the difficulty of central nervous system (CNS) regeneration, exploring effective therapeutic interventions remains daunting. Flavonoids are secondary metabolites unique to plants that have attracted attention in recent years for their potential efficacy and are now commonly used in the treatment of inflammation, tumors, and other diseases. For SCI, related studies are still exploring; some compounds, such as quercetin, fisetin, and hesperetin, have shown good anti‐inflammatory and anti‐apoptotic properties, which help to restore the function of the injured spinal cord. However, flavonoids exhibit certain disadvantages, including poor solubility, low bioavailability, and the inability to achieve long‐term controlled release. Some studies have proposed potential drug delivery strategies—including nanoparticles, hydrogels, and collagen scaffolds—to enhance efficacy. In this paper, we summarize the therapeutic mechanisms and drug delivery strategies of flavonoids in SCI by searching the relevant literature in recent years and propose future research directions to provide new ideas for the multimodal treatment of SCI.

Background: The proto‐oncogene ROS1 encodes an intrinsic type I membrane protein of the tyrosine kinase/insulin receptor family. ROS1 facilitates the progression of various malignancies via self‐mutations or rearrangements. Studies on ROS1‐directed tyrosine kinase inhibitors have been conducted, and some have been approved by the FDA for clinical use. However, the adverse effects and mechanisms of resistance associated with ROS1 inhibitors remain unknown. In addition, next‐generation ROS1 inhibitors, which have the advantage of treating central nervous system metastases and alleviating endogenous drug resistance, are still in the clinical trial stage.Method: In this study, we searched relevant articles reporting the mechanism and clinical application of ROS1 in recent years; systematically reviewed the biological mechanisms, diagnostic methods, and research progress on ROS1 inhibitors; and provided perspectives for the future of ROS1‐targeted therapy.Results: ROS1 is most expressed in malignant tumours. Only a few ROS1 kinase inhibitors are currently approved for use in NSCLC, the efficacy of other TKIs for NSCLC and other malignancies has not been ascertained. There is no effective standard treatment for adverse events or resistance to ROS1‐targeted therapy. Next‐generation TKIs appear capable of overcoming resistance and delaying central nervous system metastasis, but with a greater incidence of adverse effects.Conclusions: Further research on next‐generation TKIs regarding the localization of ROS1 and its fusion partners, binding sites for targeted drugs, and coadministration with other drugs is required. The correlation between TKIs and chemotherapy or immunotherapy in clinical practice requires further study.