Lung cancer is the leading cause of cancer-related deaths worldwide, with non-small cell lung cancer (NSCLC) accounting for 85% of all lung cancer cases. Inflammation has been proven to be one of the characteristics of malignant tumors. Chronic inflammatory response mediated by cytokines in the tumor microenvironment is an important factor in tumorigenesis. The purpose of this study was to observe and evaluate the value of red blood cell distribution width (RDW), neutrophil-to-lymphocyte ratio (NLR), and hemoglobin-to-red blood cell distribution width ratio (HRR) in the progression of NSCLC. A total of 245 patients with NSCLC, 97 patients with benign pulmonary nodules, and 94 healthy volunteers were included in this study. Factors, such as age, gender, smoking history, histological type, lymph node metastasis, distant metastasis, TNM stage, and differentiation degree were statistically analyzed. The correlation of RDW, NLR, and HRR of patients with NSCLC with other clinical experimental parameters were also analyzed. Then, the diagnostic value of RDW, NLR, and HRR in the progression of NSCLC was evaluated. RDW, NLR, and HRR could be used to distinguish patients with NSCLC from healthy controls (p < 0.05). In addition, only the RDW in the NSCLC group with III-IV stage was significantly different from that in the benign pulmonary nodules group (p = 0.033), while NLR and HRR could significantly distinguish patients with NSCLC and benign pulmonary nodules (p < 0.001). RDW and NLR were positively correlated with NSCLC stage, whereas HRR was negatively correlated with NSCLC stage. RDW, NLR, and HRR were also significantly associated with the differentiation degree of NSCLC (p < 0.05). The ROC curve analysis showed that the combination of RDW with NLR, HRR, and CEA could show significantly higher diagnostic value than any one marker alone (AUC = 0.925, 95% CI: 0.897–0.954, and sensitivity and specificity of 79.60% and 93.60%, respectively). RDW, NLR, and HRR can be utilized as simple and effective biomarkers for the diagnosis and evaluation of NSCLC progression.

BRG1 is a key factor in the process of apoptosis and oxidative damage; however, its role in the pathophysiology of ischemic stroke is unclear. Here, we discovered that during middle cerebral artery occlusion (MCAO) reperfusion in mice, microglia were significantly activated in the cerebral cortex of the infarct area, and BRG1 expression was increased in the mouse MCAO/R model, peaking at 4 days. In microglia subjected to OGD/R, BRG1 expression increased and peaked at 12 h after reoxygenation. After ischemic stroke, in vitro changing the expression of BRG1 expression levels greatly altered the activation of microglia and the production of antioxidant and pro-oxidant proteins. Knocking down BRG1 expression levels in vitro increased the inflammatory response, promoted microglial activation, and decreased the expression of the NRF2/HO-1 signaling pathway after ischemic stroke. In contrast, overexpression of BRG1 dramatically reduced the expression of NRF2/HO-1 signaling pathway and microglial activation. Our research reveals that BRG1 reduces postischemic oxidative damage via the KEAP1-NRF2/HO-1 signaling pathway, protecting against brain ischemia/reperfusion injury. Using BRG1 as a pharmaceutical target to inhibit inflammatory responses to reduce oxidative damage may be a unique way to explore techniques for the treatment of ischemic stroke and other cerebrovascular illnesses.