The Role of TLR4 on PGC-1α-Mediated Oxidative Stress in Tubular Cell in Diabetic Kidney Disease

Figure 4

HG increased TLR4 expression and activated NF-κB p65 phosphorylation in HK-2 cells. a–b: Protein levels of TLR4 in HK-2 cells following exposure to D-glucose (5.5 mM, 17.5 mM, 30 mM, and 45 mM) for 24 h (a) or D-glucose (30 mmol/L) for various times (0 h, 12 h, and 24 h) (b), and expression of NF-κB p65 and phospho-NF-κB p65 of cells exposed to 30 mM HG for indicated time points (0 h, 1 h, 2 h, and 3 h) (c) were determined by Western blot analysis. d–f: HK-2 cells were treated with TLR4 inhibitor (TAK242, 5 μM) for 2 h prior to HG (30 mM) treatment for 2 h (e) or 24 h (f) and with NF-κB blocker (parthenolide, 10 μM) and HG (30 mM) for 2 h (e) or 24 h (f), and the samples were collected for RT-PCR (d) and Western blot analysis (e–f). Each assay was representative of three independent experiments. Data were expressed as ; and .

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