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Inflammation involves in the progression of intracranial aneurysms (IAs). However, whether the neutrophil-to-lymphocyte ratio (NLR) as an inflammatory marker links to IAs stability is unidentified. This study was performed to assess the association of the NLR with IAs stability. We retrospectively reviewed the medical records of patients diagnosed with unruptured IAs from January 2014 to June 2018. According to the quartiles of the NLR, patients with unruptured IAs were categorized into four groups. We evaluated the association between the NLR and IAs stability scores and IAs growth. Multiple logistic regression models were used in the analysis. A significant dose-response association was found between the NLR with IAs stability scores and IAs growth. After adjustment for potential confounders, an elevated NLR (fourth quartile) was associated with increased PHASES score (>5) (adjusted odds ratio [OR], 2.007; 95% confidence interval [CI], 1.361–2.960; p<0.001 [p for trend <0.001]), increased ELAPSS score (>15) (adjusted OR, 1.581; 95% CI, 1.074–2.328; p=0.020 [p for trend =0.001]), increased JAPAN 3-year rupture risk score (>5) (adjusted OR, 1.512; 95% CI, 1.033–2.215; p=0.034 [p for trend <0.001]), and IAs growth (adjusted OR, 16.759; 95% CI, 3.022–92.928; p=0.001 [p for trend <0.001]). An elevated NLR was associated with increased IAs stability scores and IAs growth. The association between NLR and IAs stability need further investigate. [ABSTRACT FROM AUTHOR]

It is documented that microglia-secreted extracellular vesicles (microglia-EVs) exert neuroprotection which is important following subarachnoid hemorrhage (SAH). Herein, we focused on the mechanism of microglia-EVs harboring microRNA-140-5p (miR-140-5p) in SAH development. After the successful establishment of SAH rats, neurological function was evaluated, and behaviors were observed. Serum inflammatory factors (IL-1β and TNF-α) were quantified by ELISA, followed by the detection of microglial polarization by immunofluorescence. The relationship between miR-140-5p and monocyte to macrophage differentiation-associated (MMD) was evaluated using luciferase assay. Following the extraction of microglia and microglia-EVs, the transferring of miR-140-5p by microglia-EVs was assessed by co-culture experiments. SAH rats were treated with the EVs sourced from microglia overexpressing miR-140-5p (microglia-EVs-miR-140-5p) or EVs sourced from miR-140-5p-deficient microglia (microglia-EVs-miR-140-5p inhibitor) for in vivo effect assessment. Microglia-EVs inhibited microglia activation and secretion of TNF-α and IL-1β by delivering miR-140-5p. Microglia-EVs could transmit miR-140-5p into microglia. Furthermore, microglia-EVs-miR-140-5p reduced the expression of its target MMD, resulting in blocked inflammatory response and activation of microglia in SAH rats by disrupting the PI3K/AKT and Erk1/2 signaling. In summary, microglia-EVs transmitted miR-140-5p into microglia to downregulate MMD and finally contributed to neuroprotection in SAH rats. • MiR-140-5p is highly expressed in M-EVs and can be transferred to adjacent microglia. • Microglia-EVs-miR-140-5p inhibits microglia activation and inflammatory response. • MiR-140-5p down regulates MMD and inhibits PI3K/AKT and Erk1/2 signaling pathways. • Microglia-EVs-miR-140-5p alleviates neurological deficits of SAH rats. • This study provides a new therapeutic targets for the treatment of SAH. [ABSTRACT FROM AUTHOR]