The role and difference of TLR2 and TLR4 in rhabdomyolysis induced acute kidney injury in mice.

To investigate the role of toll like receptors (TLRs) 2 and 4 in rhabdomyolysis (RM)-related acute kidney injury (AKI). Wild-type (WT) mice and TLR2 knockout (TLR2) or TLR4 knockout (TLR4) mice were injected with either saline (sham) or glycerin (to induce RM-related AKI). Samples were collected for detection of 0 h 24 h (Cr) creatinine, urea nitrogen (BUN), creatine kinase (CK), and PAS staining of renal tissues. Serum Cr and BUN level was significantly increased in TLR2 and TLR4AKI groups more than those in the control group and the WT mice in AKI group. TLR4AKI group Cr, BUN level, and the pathological damage was lightest. The expression levels of signal transduction proteins in TLR2 and TLR4AKI group were higher than in the control group, but was lower than that in the wild AKI group, with the TLR4AKI group having the lowest levels. The expression level of inflammatory factor mRNA in TLR2 and TLR4AKI groups was higher than that in control group, but was lower than that in wild AKI group, with TLR4AKI group displaying lowest levels. Knockout of TLRs 2 and 4 decreased kidney inflammation and improved RM-related AKI.