Dai Qing, Xie Deqiong, Zhang Chenli, Zhu Lei, Xu Ying, Li Kui, Hao Wen, Yin Hefei
Department of Nephrology, The Second People's Hospital of Yibin, Yibin, China.
North Sichuan Medical College, Nanchong, China.
Front Physiol. 2021 Dec 22;12:735425. doi: 10.3389/fphys.2021.735425. eCollection 2021.
Renal ischemia-reperfusion (IR) is one of the main causes of renal injury. In severe cases with serious consequences, IR-related renal damage progresses rapidly and can even lead to acute renal failure. Its clinical treatment is currently difficult. According to various studies at home and abroad, HMGB1 is released from the nucleus into the cytoplasm or extracellular space by damaged parenchymal cells during ischemia and hypoxia, and this plays an important role in the initiation of reperfusion injury as an early inflammatory factor and is closely related to the occurrence and development of renal diseases. In recent years, the protective effect of osthole on IR of tissues and organs has been a key topic among clinical researchers. Osthole can inhibit the inflammatory response, reduce cell apoptosis the progression, and improve the prognosis of IR, thus protecting the kidney. During the development of renal IR, finding a mechanism through which the osthole blocks the release of HMGB1 from the nucleus would be helpful in detecting targets for clinical treatment.
肾缺血再灌注(IR)是肾损伤的主要原因之一。在严重情况下会产生严重后果,与IR相关的肾损伤进展迅速,甚至可导致急性肾衰竭。其临床治疗目前颇具难度。根据国内外的各项研究,高迁移率族蛋白B1(HMGB1)在缺血缺氧期间由受损的实质细胞从细胞核释放到细胞质或细胞外空间,作为一种早期炎症因子,其在再灌注损伤的起始过程中发挥重要作用,并且与肾脏疾病的发生发展密切相关。近年来,蛇床子素对组织和器官IR的保护作用一直是临床研究人员关注的重点课题。蛇床子素可抑制炎症反应,减少细胞凋亡进程,改善IR的预后,从而保护肾脏。在肾IR的发展过程中,找到蛇床子素阻断HMGB1从细胞核释放的机制将有助于探寻临床治疗靶点。