The Key Role of Inflammatory Indexes in Stroke Diagnosis and Treatment and New Research Progress

脑卒中作为一种急性脑血管疾病，严重威胁着人类的健康。近年来炎症在其发生、发展和预后中的关键作用备受关注。本文深入探讨了脑卒中与炎症指标的关系，整合多维度炎症机制，缺血性脑卒中发生后，小胶质细胞活化、补体系统激活、中性粒细胞浸润等引发炎症级联反应。经典炎症标志物如C反应蛋白(CRP)、白细胞介素-6 (IL-6)、肿瘤坏死因子α (TNF-α)等与卒中复发风险、预后分层及剂量效应关系密切；新兴炎症标志物脂蛋白相关磷脂酶A2 (Lp-PLA2)、末端补体复合物(TCC)、巨噬细胞炎症蛋白-1α (MIP-1α)等在评估斑块稳定性、预测认知功能障碍等方面具有重要价值。炎症指标在脑卒中急性期可用于早期预警，在慢性期与神经退行性变相关。在治疗上，依达拉奉右莰醇的自由基–炎症双重阻断、他汀类药物的多效性抗炎机制发挥重要作用，NLRP3炎症小体抑制剂和调节性T细胞疗法展现出良好前景。然而，炎症指标标准化检测存在障碍，个体化炎症治疗方案的探索面临挑战。未来，多组学技术有望为揭示炎症机制提供更深入的理论基础，推动脑卒中精准防治。Stroke is an acute cerebrovascular disease. Stroke, as an acute cerebrovascular disease, is a serious threat to human health. The key role of inflammation in its occurrence, development and prognosis has attracted much attention in recent years. In this paper, the relationship between stroke and inflammatory markers is explored in depth, integrating multidimensional inflammatory mechanisms. After the occurrence of ischemic stroke, microglia activation, complement system activation, and neutrophil infiltration trigger an inflammatory cascade response. Classical inflammatory markers such as C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) are closely related to stroke recurrence risk, prognostic stratification, and dose effect, while emerging inflammatory markers such as lipoprotein-associated phospholipase A2 (Lp-PLA2), terminal complement complex (TCC), and macrophage inflammatory protein-1alpha (MIP-1alpha) have been shown to be useful in assessing plaque stability and predicting cognitive function. They are valuable in assessing plaque stability and predicting cognitive dysfunction. Inflammatory indicators can be used for early warning in the acute phase of stroke and are associated with neurodegeneration in the chronic phase. Therapeutically, the dual free radical-inflammatory blockade of edaravone dextran and the pleiotropic anti-inflammatory mechanism of statins play important roles, and NLRP3 inflammatory vesicle inhibitors and regulatory T-cell therapies show good promise. However, there are obstacles to standardized testing of inflammatory indicators and challenges to the exploration of individualized inflammatory treatment protocols. In the future, multi-omics technology is expected to provide a more in-depth theoretical basis for revealing the inflammatory mechanisms and promoting the precise prevention and treatment of stroke.