The Suppression of Pin1-Alleviated Oxidative Stress through the p38 MAPK Pathway in Ischemia- and Reperfusion-Induced Acute Kidney Injury

Figure 7

Pin1 aggravates oxidative stress caused by H/R injury via activation of p38 MAPK. The H/R model was established with 12 h hypoxia and 6 h reoxygenation. The cells were transfected with si-NC or two different si-Pin1 for 24 h and then experienced the H/R process, with or without treatment with the p38 MAPK activator (5 μM). (a, b) Western blot was used to detect the expression of p-p38/p38 after Pin1 silence and quantification was performed. (c, d) The expression of p-p38/p38 after Pin1 silence and its quantification, with or without treatment with the p38 MAPK activator. (e–i) Western blot was used to detect the expression of Pin1, 4-HNE, COX2, and MPO and quantification was performed. (j–m) The SOD, MDA, ROS, and H₂O₂ levels were detected (). The values were presented as . vs. the control group; vs. the si-Pin1-1 group; vs. the si-Pin1-2 group.

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