Therapeutic effect and mechanism of 4-phenyl butyric acid on renal ischemia-reperfusion injury in mice

xlomafota13 shared this article with you from Inoreader Therapeutic effect and mechanism of 4-phenyl butyric acid on renal ischemia-reperfusion injury in mice Via Experimental and therapeutic medicine Exp Ther Med. 2022 Feb;23(2):144. doi: 10.3892/etm.2021.11067. Epub 2021 Dec 15. ABSTRACT The aim of the present study was to explore the effects and possible mechanism of 4-phenylbutyric acid (4-PBA) on renal ischemia-reperfusion injury (RIRI) in mice. A RIRI model of HK-2 cells was constructed using hypoxia/reoxygenation (H/R) treatment. Dexmedetomidine and 4-PBA were used to treat the cells before and after modeling. Apoptosis and expression levels of cyclophilin D (CypD), cytochrome c, eukaryotic translation initiation factor 2α (eIF2α), glucose-regulated protein 78 (GRP78), intercellular adhesion molecule (ICAM)-1 and vascular adhesion molecule (VCAM)-1 were measured using flow cytometry, western blotting and immunohistochemistry. The renal volume, weight and renal arterial resistance index (RRI) were determined using the renal ischemia model. Compared with untreated model cells, 4-PBA treatment significantly decreased ap optosis and the expression levels of CypD, Cytochrome c, eIF2α and GRP78 in HK-2 cells. There was no significant change in renal volume and weight after modeling, but RRI was significantly decreased after 4-PBA treatments in the model. Western blotting and immunohistochemistry analysis demonstrated that 4-PBA treatment also significantly decreased the expression of ICAM-1 and VCAM-1. Overall, 4-PBA had a therapeutic effect on RIRI in mice. This protection may be mediated by decreasing the expression levels of CypD, Cytochrome c, eIF2α and GRP78, and subsequent reduction of cellular oxygen free radicals and apoptosis, leading to an alleviated endoplasmic reticulum stress response and RIRI. PMID:35069825 | PMC:< a href="https://www.ncbi.nlm.nih.gov/pmc/PMC8756420/?utm_source=Inoreader&utm_medium=rss&utm_content=1ba2t84FK1dz-fAY5g7-lbp7yzA9oSsgU2XptRGyGkyx-wIkEA&ff=20220125000243&v=2.17.5" target="_blank" rel="noopener" class="underlink bluelink">PMC8756420 | DOI:10.3892/etm.2021.11067 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.