CBLB502，一种来自沙门氏菌鞭毛蛋白的Toll样受体-5（TLR-5）激动剂，在哺乳动物组织中对辐射和化学药物起到保护作用并刺激组织再生。本研究旨在探讨CBLB502是否可以保护化疗药物顺铂（CDDP）引起的肝脏和肾脏损伤，并揭示其保护效应的潜在机制。实验中，小鼠在CDDP（20 mg/kg，腹腔注射）给药前0.5 h进行CBLB502（0.2 mg/kg，腹腔注射）预处理，然后分析肝肾指标、血液生化指标和组织病理学。结果显示，CBLB502预处理缓解了CDDP引起的肝肾损伤。RNA测序和生物信息学分析表明，CDDP在肝肾中诱导了类似的损伤促进基因调控模式。CBLB502主要通过不同的途径保护了CDDP诱导的肝肾损伤。然而，一些CBLB502调控的基因在肝肾中是共同的，包括与血凝、纤溶、止血、细胞凋亡调控、NF-kappaB信号通路以及对脂多糖的响应相关的基因，提示了CBLB502的普遍保护效应。本研究数据揭示了CBLB502对CDDP引起的肝肾组织损伤的保护机制，并为进一步研究功能基因和调控机制提供了基础，这些功能基因和调控机制可介导对于化疗和放疗引起的损伤的保护作用。版权所有©2023，国际抗癌研究协会（George J. Delinasios博士），保留所有权利。

CBLB502, a Toll-like receptor-5 agonist derived from Salmonella flagellin, exerts protective roles against irradiation and chemical drugs in mammalian tissues and stimulates tissue regeneration. This study aimed to investigate whether CBLB502 can protect against liver and kidney damage induced by the chemotherapeutic drug cisplatin (CDDP) and the underlying mechanism of the protective effect.Mice were pretreated with CBLB502 [0.2 mg/kg, intraperitoneal (i.p.) injection] 0.5 h prior to administration of CDDP (20 mg/kg, i.p. injection), and analyses of the liver and kidney indices, blood biochemistry, and histopathology were performed.Pretreatment with CBLB502 alleviated CDDP-induced liver and kidney damage. RNA sequencing and bioinformatic analysis indicated that CDDP induced a similar damage-promoting gene regulation pattern in the liver and kidney. CBLB502 protected against liver and kidney damage only after CDDP treatment primarily via different pathways. However, some CBLB502-regulated genes were common between the liver and kidney, including those involved in blood coagulation, fibrinolysis, hemostasis, apoptotic regulation, NF-kappaB signaling, and response to lipopolysaccharide, suggesting a general protective effect by CBLB502.Our data provide insights into the protective mechanism of CBLB502 against CDDP-induced tissue damage in the liver and kidney and might provide a basis for future studies on functional genes and regulatory mechanisms that mediate protection against chemoradiotherapy-induced damage.Copyright © 2023, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.