Skip to main content
. 2015 Nov 23;21(1):886–899. doi: 10.2119/molmed.2015.00196

Figure 6.

Figure 6

The involvement of PI3K and phospho-Akt in the PPARα-induced NHE1 signaling pathway. (A) The influence of wortmannin on gentamicin-induced apoptotic signals in the pcPPAR-transfected NRK-52E cells. NRK-52E cells were transfected with pcPPAR or blank vectors, pretreated with or without 1 nmol/L wortmannin (a PI3K inhibitor) for 30 min and then treated with or without 3 mmol/L gentamicin for 24 h. Total proteins of the transfected cells were analyzed by Western blotting with the specific antibodies as indicated. GAPDH was used as a loading control. Relative increases in the protein bands are also presented in a bar chart form. Results are means ± SD (n = 3). *P < 0.05 versus the blank vector group without any treatment. #P < 0.05 versus the blank vector group with gentamicin treatment. **P < 0.05 versus the pcPPAR group with gentamicin treatment. Statistical differences between the two groups were determined using the Student t test. (B) The influence of cariporide on PI3K expression in the pcPPAR-transfected cells. The pcPPAR-transfected cells were pretreated with 1 μmol/L cariporide for 30 min and then treated with or without 3 mmol/L gentamicin. PI3K in each sample was detected by Western blotting. Relative increases in the protein bands are also presented in a bar chart form. Results are means ± SD (n = 3). *P < 0.05 versus the blank vector group without any treatment (by Student t test).