Elafibranor Inhibits Chronic Kidney Disease Progression in NASH Mice
Figure 5
Chronic elafibranor treatment suppressed the progression of CKD through the inhibition of renal oxidative stress/apoptosis in HFD mice with steatohepatitis. (a) Albuminuria (urine albumin, µg/day); (b) urinary albumin-to-creatinine ratio (ACR, albumin µg/mg of creatinine); (c) glomerular filtration rate (GFR, µL/min); (d) urine output; (e) urine 8-isoprostane (ng/mg cr) secretion; (f) serum caspase 3/7 activity; (g) histologic images/bar graphs of severity of renal injury. Renal tubular damage was assessed using a tubular damage score including atrophy and flattening of proximal tubule epithelial cells, and tubular dilation: 0 = normal; 1 = <20%; 2 = 20 to 40%; 3 = 40 to 60%; 4 = 60 to 80%; and 5 = 80%. The features of tubulointerstitial fibrosis include tubular atrophy/dilatation, presence of mononuclear inflammatory cells, widening of interstitial spaces with deposition of extracellular matrix, interstitial cell proliferation and wrinkling or thickened tubular basement membrane. p<0.05 versus NC-group; p<0.05, 0.01 versus HFD-group; †p<0.05 versus HFD-elaf group.