Background: Ischemic stroke (IS) is a common neurological disease in the elderly, but the relationship between neutrophil/albumin ratio (NAR) and leukocyte count/albumin ratio (LAR) and the severity of neurological function injury and early neurological deterioration (END)occurrence remain elusive in acute IS.Methods: A total of 299 patients with acute IS and 56 healthy controls were enrolled. According to the NIHSS score at admission, the disease group was divided into three groups (mild, moderate and severe IS), and the differences in ve indexes NAR, LAR, neutrophil count, leukocyte count and albumin among the four groups were analyzed. Furthermore, explore the correlation between the above indicators and the severity of IS and END occurrence.Results: The results showed that higher NAR, LAR, neutrophil count, leukocyte count levels and lower albuminlevels were associated with acute IS, and the levels of NAR and LAR increased gradually in three groups of IS. NAR and LAR were positively and albumin was negatively correlated with the severity of IS.Meanwhile, NAR and LAR showed a good predictive value in identifying patients with END after acute IS.Conclusions: NAR and LAR may be predictors of the severity of IS and END occurrence after acute IS.

Background: Ischemic stroke (IS) is a common neurological disease in the elderly, but the relationship between neutrophil/albumin ratio (NAR) and leukocyte count/albumin ratio (LAR) and the severity of neurological function injury and early neurological deterioration (END)occurrence remain elusive in acute IS. Methods: A total of 299 patients with acute IS and 56 healthy controls were enrolled. According to the NIHSS score at admission, the disease group was divided into three groups (mild, moderate and severe IS), and the differences in five indexes NAR, LAR, neutrophil count, leukocyte count and albumin among the four groups were analyzed. Furthermore, explore the correlation between the above indicators and the severity of IS and END occurrence. Results: The results showed that higher NAR, LAR, neutrophil count, leukocyte count levels and lower albuminlevels were associated with acute IS, and the levels of NAR and LAR increased gradually in three groups of IS. NAR and LAR were positively and albumin was negatively correlated with the severity of IS. Meanwhile, NAR and LAR showed a good predictive value in identifying patients with END after acute IS. Conclusions: NAR and LAR may be predictors of the severity of IS and END occurrence after acute IS.

Background The acute inhibition of glymphatic after stroke has been shown to aggravate post-stroke inflammation and apoptosis; however, the related mechanisms remain ambiguous. This study aimed to assess the specific mechanism of inflammation and apoptosis after cerebral ischemia-reperfusion (I/R) injury by improving glymphatic dysfunction. Materials and Methods Ischemic stroke was induced using the mice middle cerebral artery occlusion (MCAO) model. The C57/BL6 mice were randomly divided into three groups as follows: sham operation, Ischemia-reperfusion (I/R) 48 hours, and N-(1,3,4-thiadiazol-2-yl) pyridine-3-carboxamide dihydrochloride (TGN-020) + I/R 48 hours treatment. Neurological examination, TTC, fluorescence tracer, western blot, and immunofluorescence staining were performed in all mice in sequence. The glymphatic function in the cortex surrounding cerebral infarction was determined using tracer, glial fibrillary acid protein (GFAP), aquaporin-4 (AQP4) co-staining, and beta-amyloid precursor protein (APP) staining, differential genes were detected using RNA-seq. Iba-1, IL-1β, TNF-α, cleaved caspase 3, and tunel staining were used to verify inflammation and apoptosis after TGN-020 treatment. Results Compared with I/R group, the degree of neurological deficit was alleviated in TGN-020 group. TGN-020 alleviated glymphatic dysfunction by improving astrocyte proliferation and reducing tracer accumulation in the peri-infarct area. RNA-seq showed that the differentially expressed genes were mainly involved in the activation of astrocytes and microglia, and involved in the ERK pathway. RNA-seq was verified by western blot and immunofluorescence. Conclusions The inflammation of astrocytes and microglia after cerebral ischemia-reperfusion (I/R) is closely related to the glymphatic system. The improvement of glymphatic function may play a neuroprotective role after cerebral I/R by inhibiting inflammation through ERK pathway.

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