Figure 5
From: Quantitating intracellular oxygen tension in vivo by phosphorescence lifetime measurement
Phosphorescence lifetime change and proof of hypoxia in chronic damaged kidney.
(a) Experimental scheme of unilateral ischemia-reperfusion model. (b) Average of phosphorescence lifetime of I/R injured and contralateral kidneys. Values under the graph show converted pO2 (mmHg) from phosphorescence lifetime by using the calibration line. n = 5. Error bar: S.D. #P < 0.05 by two-tailed paired t-test. (c,d) Pimonidazole protein adducted immunohistochemistry of I/R injured model. Histological image of pimonidazole staining of I/R injured kidney (c, right panel) and contralateral kidney (c, left panel) are shown. More tubules in I/R injured kidneys are positive for pimonidazole adduct protein staining (representatives were indicated by arrows), which is supported by quantitative analysis of the proportion of stained tubules (d, n = 7). Original magnifications, 400×. Brightness and contrast were adjusted from original images. Scale bar: 30 μm. Error bar: S.D. #P < 0.05 in two-tailed paired t-test. (e,f) Assessment of peritubular capillary (PTC) density using anti-CD31 antibody. Histological images of CD-31 staining of I/R injured kidney (e, right panel) and contralateral kidney (e, left panel) were shown. Disruption and distortion of PTC was seen (arrowhead). Quantitative analysis of rarefaction index shows the decrease in PTC in I/R injured kidney (f, n = 7). Original magnifications, 400×. Brightness and contrast were adjusted from original image. Scale bar: 30 μm. Error bar: S.D. #P < 0.05 in two-tailed paired t-test.
