The Protective Effect of a Newly Developed Molecular Chaperone– Inducer Against Mouse Ischemic Acute Kidney Injury

• Published in: Journal of Pharmacological Sciences Vol. 109; no. 2; pp. 311 - 314
• Main Authors: Prachasilchai, Worapat, Sonoda, Hiroko, Yokota-Ikeda, Naoko, Ito, Katsuaki, Kudo, Takashi, Imaizumi, Kazunori, Ikeda, Masahiro
• Format: Journal Article
• Language: English
• Published: Japan Elsevier B.V 2009; The Japanese Pharmacological Society; Elsevier
• Subjects: Animals; endoplasmic reticulum (ER) stress; Heat-Shock Proteins - genetics; Heat-Shock Proteins - metabolism; Ischemia - drug therapy; Kidney - injuries; Male; Mice; Mice, Inbred Strains; Molecular Chaperones - genetics; Molecular Chaperones - metabolism; renal ischemia-reperfusion injury; Reperfusion Injury - prevention & control; RNA, Messenger - metabolism; Thiocyanates - therapeutic use; Transcriptional Activation; Tunicamycin - administration & dosage; Tunicamycin - pharmacology; unfolded protein response; Up-Regulation; unfolded protein response; endoplasmic reticulum (ER) stress; renal ischemia-reperfusion injury
• ISSN: 1347-8613; 1347-8648
• DOI: 10.1254/jphs.08272SC

Activation of the unfolded protein response (UPR) has been suggested to attenuate renal ischemia-reperfusion (I/R) injury. We recently found a compound, namely BIX, that activated the UPR selectively through the activating transcription factor 6 pathway. This study examined the effect of BIX on renal I/R injury in mice. BIX selectively up-regulated renal BiP mRNA and protein. Pretreatment with BIX significantly ameliorated renal I/R injury. Coadministration of BIX and tunicamycin, a non-selective UPR inducer, provided no additional protection. Our results suggest that the UPR activation by BIX leads to a novel drug therapy against renal I/R injury.