中医药靶向调控炎症相关信号通路防治慢性阻塞性肺疾病急性加重的研究进展OA

Acute exacerbation of chronic obstructive pulmonary disease(AECOPD)constitutes the acute deterioration phase of chronic obstructive pulmonary disease(COPD),typified by an abrupt intensification of respiratory symptomatology,encompassing exacerbated dyspnea,heightened cough severity,augmented sputum volume,and pronounced respiratory insufficiency.Systemic inflammatory cascades serve as a cardinal etiological driver of AECOPD,emanating from multifaceted host-pathogen interactions involving viral,bacterial,or polymicrobial infections,superimposed upon environmental modulators that collectively precipitate accelerated pathological progression.These contributory elements markedly escalate the inflammatory milieu within the small airways,surmounting endogenous anti-inflammatory safeguards,thereby precipitating airway epithelial barrier disruption,microvascular dilation,edema,and prolific immune cell infiltration,which in turn perpetuate an inflammatory amplification loop.Such mechanisms converge to synergistically impair pulmonary function and extend durations of inpatient care.Current therapeutic paradigms for AECOPD predominantly incorporate bronchodilators,anti-inflammatory pharmacotherapies,supplemental oxygen administration,and mechanical ventilatory support.Notwithstanding these interventions,persistent limitations include the adverse sequelae of protracted systemic glucocorticoid therapy,escalating antimicrobial resistance profiles,and ventilator-associated morbidities.Ergo,there exists an imperative to investigate novel therapeutic modalities that confer enhanced safety and efficacy.TCM proffers salient therapeutic merits via its multi-target and multi-pathway pharmacodynamics,facilitating regulation of pivotal signaling pathways,including the Toll-like receptor 4(TLR4)/nuclear factor-κB(NF-κB),NF-κB/NOD-like receptor pyrin domain containing 3(NLRP3),phosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt),Janus kinase(JAK)/signal transducer and activator of transcription(STAT),and neutrophil elastase(NE)/mucin 5AC(MUC5AC)pathways.Through such regulatory interventions,TCM efficaciously attenuates inflammatory response,ameliorates symptomatic burden,and diminishes the incidence of AECOPD.The present investigation endeavors to delineate systematically the extant advancements in TCM-mediated regulation of inflammation-related signaling pathways within the context of AECOPD,thereby furnishing a robust theoretical framework and empirical guidance for optimized clinical interventions and pharmaceutical innovations in AECOPD management.