Abstract：
Ischemic stroke (IS) is one of the leading causes of death and disability. Its pathogenesis is not completely clear, and inflammatory cascade is one of its main pathological processes. The current clinical practice of IS is to restore the blood supply to the ischemic area after IS as soon as possible through thrombolytic therapy to protect the vitality and function of neurons. However, blood reperfusion further accelerates ischemic damage and cause ischemia-reperfusion injury. The pathological process of cerebral ischemia-reperfusion injury involves multiple mechanisms, and the exact mechanism has not been fully elucidated. Pyroptosis, a newly discovered form of inflammatory programmed cell death, plays an important role in the initiation and progression of inflammation. It is a pro-inflammatory programmed death mediated by caspase Caspase-1/4/5/11, which can lead to cell swelling and rupture, release inflammatory factors IL-1β and IL-18, and induce an inflammatory cascade. Recent studies have shown that pyroptosis and its mediated inflammatory response are important factors in aggravating ischemic brain injury, and inhibition of pyroptosis may alleviate the ischemic brain injury. Furthermore, studies have found that natural plant components may have a regulatory effect on pyroptosis. Therefore, this review not only summarizes the molecular mechanism of pyroptosis and its role in ischemic stroke, but also the role of natural plant components as regulator of pyroptosis, in order to provide reference information on pyroptosis for the treatment of IS in the future.
摘要：
缺血性中风（IS）是导致死亡和残疾的主要原因之一。其发病机制尚未完全明确,炎症级联反应是其主要病理过程之一。目前IS的临床实践是通过溶栓治疗尽快恢复IS后缺血区的血供,以保护神经元的活力和功能。然而,血液再灌注进一步加速缺血损伤并引起缺血再灌注损伤。脑缺血再灌注损伤的病理过程涉及多种机制,确切的机制尚未完全阐明。焦亡,一种新发现的炎症程序性细胞死亡形式，在炎症的开始和进展中起着重要作用。它是由caspasecaspase-1/4/5/11介导的促炎程序性死亡，可导致细胞肿胀和破裂，释放炎症因子IL-1β和IL-18，并诱导炎症级联反应。最近的研究表明，焦凋亡及其介导的炎症反应是加重缺血性脑损伤的重要因素，抑制焦亡可以减轻缺血性脑损伤。此外，研究发现，天然植物成分可能对焦亡具有调节作用。因此,本文综述了焦凋亡的分子机制及其在缺血性脑卒中中的作用,以及天然植物成分作为焦亡调节剂的作用，以期为今后IS的治疗提供有关焦亡的参考信息。
