Negative Regulation of Tec Kinase Alleviates LPS-Induced Acute Kidney Injury in Mice via theTLR4/NF-κB Signaling Pathway

Figure 6

Effects of LFM-A13 or Tec-siRNA on the expression of the NF-κB pathway and TLR4/MyD88 in LPS-induced AKI or LPS-stimulated NRK-52E cell. Protein extracts were obtained from kidney tissues and NRK-52E cells, and protein expression level was detected by Western blot analysis. (a, b) Expressions of NF-κB p65 and p-p65 in kidney tissues were analyzed by Western blot. The relative expression of p-p65 was quantified with a densitometry. LFM-A13 pretreatment inhibited the activity of NF-κB p-p65. (c, d) Expressions of NF-κB p65, p-p65, IκBα, and p-IκBα in NRK-52E cell were detected by immunoblotting. The relative levels were quantified. LPS promoted phosphorylation of NF-κB p65, while Tec-siRNA protected degradation of IκBα and inhibited phosphorylation status of p65 and IκBα. (e, f) Expressions of TLR4 and MyD88 were detected and quantified. LFM-A13 pretreatment reduced LPS-induced TLR4/MyD88 expression. Densitometric analysis of the results expressed as arbitrary units of the of each group. , . .

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