Fig. 6. Role of OPC in the PI3K/AKT and NF
κB signaling pathways against LPS-induced renal tubular injury. (A) Expression of PI3K/AKT signaling pathways in LPS-induced renal tubular injury. Mouse tubular epithelial cells (MTEC) were treated with LPS (5 μg/ml) + ATP (3 mM) in a time-dependent manner. Cell lysates were obtained for Western blotting analysis of p-PI3K, PI3K, p-AKT, and AKT. (B) Analyzing A for a semi-quantitative densitometric ratio of p-PI3K to total-PI3K and p-AKT to total-AKT (n = 3). (C) The influence of OPC on the expression of the PI3K/AKT signaling pathway in MTEC cells, MTEC cells were treated with OPC (5 μM) for 1 h before being exposed to LPS (5 μg/ml) + ATP (3 mM) for 24 h. Cell lysates were obtained for the Western blotting analysis of p-PI3K, PI3K, p-AKT, and AKT. (D) Analyzing C for a semi-quantitative densitometric ratio of p-PI3K to total-PI3K and p-AKT to total-AKT (n = 3). (E) Expression of NFκB signaling pathway induced by LPS In a 6-well plate, MTEC cells were treated with LPS (5 μg/ml) + ATP (3 mM) in a time-dependent manner. Cell lysates were obtained for Western blotting analysis of p-IKKα/β, p-NFκB, NFκB, and GAPDH. (F) Analyzing E for a semi-quantitative densitometric ratio of p-NFκB to total-NFκB and p-IKKα/β to GAPDH (n = 3). (G) The influence of OPC on the expression of NFκB signaling pathway in MTEC cells. MTEC cells were treated with OPC (5 μM) for 1 h before being exposed to LPS (5 μg/ml) + ATP (3 mM) for 24 h. Cell lysates were obtained for the Western blotting analysis of p-IKKα/β, p-NFκB, NFκB, and GAPDH. (H) Analyzing G for a semi-quantitative densitometric ratio of p-NFκB to total-NFκB and p-IKKα/β to GAPDH (n = 3). The p-values are indicated at the top of the bars. OPC, oligomeric proanthocyanidin; LPS, lipopolysaccharide; NFκB, nuclear factor κB; Ctrl, control. #p < 0.05, ##p < 0.01, ###p < 0.001 versus control. *p < 0.05 and **p < 0.01 versus LPS, respectively.
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