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2.
Figure 6

Figure 6. Effect of ROS on expression of MAPK and Akt in kidneys of rats postburn.. From: Sustained Oxidative Stress Causes Late Acute Renal Failure via Duplex Regulation on p38 MAPK and Akt Phosphorylation in Severely Burned Rats.

(AB) Tempol attenuated ROS-induced phosphorylation of p38 and inhibition of Akt at 72 h postburn. (CD) Induction of ROS with tBHP significantly increased p38 but inhibited Akt phosphorylation. **P<0.01 vs. Sham; ##P<0.01 vs. Vehicle. n = 6 rats per group.

Yafei Feng, et al. PLoS One. 2013;8(1):e54593.
3.
Figure 5

Figure 5. Expression of MAPK and Akt signaling in kidneys of rats postburn.. From: Sustained Oxidative Stress Causes Late Acute Renal Failure via Duplex Regulation on p38 MAPK and Akt Phosphorylation in Severely Burned Rats.

Burn induced (A–C) elevated renal p38 MAPK phosphorylation in a time dependent manner but had no significant effect on ERK or JNK, whereas (D) Akt phosphorylation increased during the first 24 h but decreased beginning from 48 h after burn. **P<0.01 vs. Sham. n = 6 rats per group per time point.

Yafei Feng, et al. PLoS One. 2013;8(1):e54593.
4.
Figure 2

Figure 2. Histopathological renal injury in rats at 72 h after burn.. From: Sustained Oxidative Stress Causes Late Acute Renal Failure via Duplex Regulation on p38 MAPK and Akt Phosphorylation in Severely Burned Rats.

Representative images (magnification  = 200×) showed the histological examination for tubular damage with different treatments postburn using periodic acid–Schiff (PAS) staining. The data indicated burn induced significant renal damage at 72 h, which was improved by inhibiting ROS production or p38 MAPK expression, and deteriorated by inhibiting Akt expression. **P<0.01 vs. Sham; #P<0.05, ##P<0.01 vs. Vehicle. n = 6 rats per group per time point.

Yafei Feng, et al. PLoS One. 2013;8(1):e54593.
5.
Figure 1

Figure 1. Blood urea nitrogen (BUN) and creatinine in rats after burn.. From: Sustained Oxidative Stress Causes Late Acute Renal Failure via Duplex Regulation on p38 MAPK and Akt Phosphorylation in Severely Burned Rats.

Analysis of burn-induced late renal dysfunction evidenced by BUN and creatinine (A–B) at different time points of 3 h, 6 h, 24 h, 48 h and 72 h and (C–D) with different treatments at 72 h postburn. The data showed that burn induced a late renal dysfunction at 72 h, which was improved by inhibiting reactive oxygen species (ROS) or p38 MAPK with tempol or SB203580, and deteriorated by inhibiting Akt expression at 72 h. Treatment with tBHP also caused significant renal dysfunction. *P<0.05, **P<0.01 vs. Sham; #P<0.05, ##P<0.01 vs. Vehicle. n = 6 rats per group per time point.

Yafei Feng, et al. PLoS One. 2013;8(1):e54593.
6.
Figure 3

Figure 3. Tubular cell apoptosis and caspase-3 activation in rats after burn.. From: Sustained Oxidative Stress Causes Late Acute Renal Failure via Duplex Regulation on p38 MAPK and Akt Phosphorylation in Severely Burned Rats.

Burn induced (A) tubular apoptosis presented by renal TUNEL staining (magnification  = 400×) and increased caspase-3 activation (B) at different time points of 3 h, 6 h, 24 h, 48 h and 72 h (C) with different treatments at 72 h postburn. The data showed that burn induced increased caspase-3 activation and tubular cell apoptosis at a relatively late time stage postburn. Inhibition of ROS production and p38 MAPK phosphorylation alleviated renal apoptotic injury, while blockage of Akt expression aggravated the apoptosis in late renal failure after burn. Administration of tBHP led to obvious apoptotic kidney injury. **P<0.01 vs. Sham; #P<0.05, ##P<0.01 vs. Vehicle (72 h). n = 6 rats per group per time point.

Yafei Feng, et al. PLoS One. 2013;8(1):e54593.
7.
Figure 4

Figure 4. Induction of oxidative stress in kidneys of rats postburn.. From: Sustained Oxidative Stress Causes Late Acute Renal Failure via Duplex Regulation on p38 MAPK and Akt Phosphorylation in Severely Burned Rats.

Burn injury induced sustained ROS generation evidenced by increased renal (A) H2O2 production, (B) thiobarbituric acid-reactive substances (TBARS) generation, suppressed antioxidant activity evidenced by decreased (C) SOD level and at 3 h, 6 h, 24 h, 48 h and 72 h after burn, which were attenuated by tempol at 72 h after burn. Renal (D) MnSOD activity and (E) protein expression, and (F) Nox4 expression was analyzed to determine the mitochondrial status. Treatment with tBHP also induced significant oxidative stress in kidneys of sham rats. *P<0.05, **P<0.01 vs. Sham; ##P<0.01 vs. Vehicle (72 h). n = 6 rats per group per time point.

Yafei Feng, et al. PLoS One. 2013;8(1):e54593.

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