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• W2163800490 abstract "It has been shown that the inhibition of the Rho/Rho kinase (ROCK) pathway prevents tubulointerstitial fibrosis and ameliorates renal function in various progressive renal disorders. The present study was to determine whether fasudil, a ROCK inhibitor, has a protective effect on cyclosporine A (CsA)-induced nephropathy. Male Sprague-Dawley rats were treated with CsA (<i>n</i> = 10, 20 mg · kg⁻¹ day⁻¹ s.c.), CsA + fasudil (<i>n</i> = 10, 3 mg · kg⁻¹ day⁻¹ i.p.), or vehicle alone (<i>n</i> = 10) for 28 days. Fasudil cotreatment ameliorated CsA-induced changes and restored renal function. CsA decreased the expression of endothelial nitric-oxide synthase and increased inducible nitric-oxide synthase/3-nitrotyrosine in the kidney. Accordingly, there was infiltration of inflammatory cells and up-regulation of inflammatory cytokines. Fasudil also significantly suppressed the expression of transforming growth factor-β1, Smad signaling, and subsequent epithelial-to-mesenchymal processes. In addition, fasudil augmented p27^kip1 expression and decreased the number of proliferating cell nuclear antigen-positive cells. In another series of experiments using HK-2 cells in culture, fasudil also suppressed CsA-induced increases in mitogen-activated protein kinase phosphorylation. CsA induced expression of p53, the degree of which was attenuated by fasudil in association with decreases of proapoptotic markers such as Bad, Bax, and total/cleaved caspase-3. These results suggest that inhibition of the Rho/ROCK pathway attenuates CsA-induced nephropathy through the suppression of the induction of inflammatory, apoptotic, and fibrogenic factors, along with inhibition of Smad, mitogen-activated protein kinases, and nitric oxide signaling pathways." @default.
• W2163800490 created "2016-06-24" @default.
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• W2163800490 date "2011-04-07" @default.
• W2163800490 modified "2023-09-24" @default.
• W2163800490 title "Rho Kinase Inhibition by Fasudil Attenuates Cyclosporine-Induced Kidney Injury" @default.
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• W2163800490 doi "https://doi.org/10.1124/jpet.111.179457" @default.
• W2163800490 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21474569" @default.
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