Research Progress on the Multitarget Mechanisms of Terpenoids in the Treatment of Ischemic Stroke

Cerebral ischemic stroke (CIS) is an acute cerebrovascular disease associated with high morbidity and disability rates. It is characterized by neurological damage caused by the interruption of cerebral blood flow, often accompanied by sequelae such as motor dysfunction and cognitive decline, which seriously affect the quality of life of patients. Despite continuous advancements in treatment methods, challenges persist, such as time window constraints, limited efficacy, and potential adverse reactions. Therefore, finding more proactive and effective treatment approaches has become an urgent problem to be solved. The mechanism of action of terpenoids is not a simple single-target inhibition. Essentially, it lies in the systematic remodeling of the postischemic neural microenvironment. The pathophysiological process of CIS involves complex cascades, including energy failure, excitotoxicity, oxidative stress, neuroinflammation, disruption of the blood-brain barrier, multiple cell death pathways, mitochondrial dysfunction, and impairment of nerve repair. Terpenoids can intervene in ischemic stroke through a dual-mechanism approach of direct neuroprotection and indirect microenvironment regulation by targeting key nodes within the abovementioned pathological network, ultimately achieving the protection and restoration of neural function. The aim of this review was to deepen the understanding of the therapeutic value of terpenoids in stroke; from an integrated perspective, it revealed the scientific essence of the multitarget synergistic effects of natural products, thereby providing a theoretical cornerstone and an innovative direction for the development of next-generation drugs for treating stroke.