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. 2019 Dec 20;30:101411. doi: 10.1016/j.redox.2019.101411

Fig. 7.

Fig. 7

Role of the PKC pathway in salusin-β-induced oxidative stress in renal tubular cells. (A) Effect of salusin-β knockdown on the phosphorylated PKC in HK-2 cells treated either cisplatin or LPS. (B) Effect of salusin-β overexpression on the phosphorylated PKC in HK-2 cells treated either cisplatin or LPS. HK-2 cells were pretreated with PKC inhibitor Go 6976 (5 μM), and then transfected with lentivirus expressing salusin-β (MOI = 100) for 48 h. The protein expressions of GTP-Rac1 (C), p22phox (D), NOX-4 (E), and p47phox (F) were measured. (G&H) The membrane and cytosol level of p47phox were also detected. (I) Activities of SOD and GSH. (J) 15-F2t-isoprostane and 8-iso-PGF-2α levels. Values are mean ± SE. *P < 0.05 vs. Control, †P < 0.05 vs. Cisplatin or Salusin-β. ‡P < 0.05 vs. LPS. n = 6 for each group.