Skip to main content


Figure 4 | Cell Communication and Signaling

Figure 4

From: A p38MAPK/MK2 signaling pathway leading to redox stress, cell death and ischemia/reperfusion injury

Figure 4

p38MAPK (p38) inhibition prevents ischemia/reperfusion-induced increase in the serum levels of kidney function markers and oxidative stress indicators. Serum levels of creatinine (A) and urea (B) were measured on indicated days (D0 to D7) following IR in rats pretreated with either BIRB796 (B-796) at two different doses (5 mg or 20 mg/kg BW) or vehicle (DMSO) only. Day 0 represents measurements before ischemia in every group. Likewise, serum cystatin C (C) and NGAL (D) levels were measured on indicated days of reperfusion in another set of experiments where rats were pretreated with either BIRB796 (B-796) (5 mg/kg BW) or DMSO only. Results are given as mean ± SEM (n = 4-7). *p < 0.05, **p < 0.01 ***p < 0.001, difference between DMSO- and BIRB796-treated groups at the given time points. (E-H) Rats were pretreated with BIRB796 (B-796) (5 mg/kg BW) for 1 hour and subjected to 1 hour of renal ischemia followed by different time points of reperfusion (15 min, 2 days, 7 days). Kidneys were harvested at given time points of reperfusion and total tissue lysates were used to determine the expression level of HSP70 (E), the abundance of 3-nitrotyrosine (3-Nitrotyr) (F) and 4-HNE modified proteins (G), and the phosphorylation of H2AX (H). Results are given as mean ± SEM (n = 3-4). $p < 0.01, Øp < 0.05 vs. sham-operated group, **p < 0.01 vs. IR-15 min group, §p < 0.01, #p < 0.05 vs. IR-2d group, *p < 0.05 vs. IR-7d group.

Back to article page