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Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Chin+Med+J+(Engl) 2017 ; 130 (18): 2163-9 Nephropedia Template TP
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Pharmacological Inhibition of Macrophage Toll-like Receptor 4/Nuclear Factor-kappa B Alleviates Rhabdomyolysis-induced Acute Kidney Injury #MMPMID28836571
Huang RS; Zhou JJ; Feng YY; Shi M; Guo F; Gou SJ; Salerno S; Ma L; Fu P
Chin Med J (Engl) 2017[Sep]; 130 (18): 2163-9 PMID28836571show ga
Background:: Acute kidney injury (AKI) is the most common and life-threatening systemic complication of rhabdomyolysis. Inflammation plays an important role in the development of rhabdomyolysis-induced AKI. This study aimed to investigate the kidney model of AKI caused by rhabdomyolysis to verify the role of macrophage Toll-like receptor 4/nuclear factor-kappa B (TLR4/NF-?B) signaling pathway. Methods:: C57BL/6 mice were injected with a 50% glycerin solution at bilateral back limbs to induce rhabdomyolysis, and CLI-095 or pyrrolidine dithiocarbamate (PDTC) was intraperitoneally injected at 0.5 h before molding. Serum creatinine levels, creatine kinase, the expression of tumor necrosis factor (TNF)-?, interleukin (IL)-1? and IL-6, and hematoxylin and eosin stainings of kidney tissues were tested. The infiltration of macrophage, mRNA levels, and protein expression of TLR4 and NF-?B were investigated by immunofluorescence double-staining techniques, reverse transcriptase-quantitative polymerase chain reaction, and Western blotting, respectively. In vitro, macrophage RAW264.7 was stimulated by ferrous myoglobin; the cytokines, TLR4 and NF-?B expressions were also detected. Results:: In an in vivo study, using CLI-095 or PDTC to block TLR4/NF-?B, functional and histologic results showed that the inhibition of TLR4 or NF-?B alleviated glycerol-induced renal damages (P < 0.01). CLI-095 or PDTC administration suppressed proinflammatory cytokine (TNF-?, IL-6, and IL-1?) production and macrophage infiltration into the kidney (P < 0.01). Moreover, in an in vitro study, CLI-095 or PDTC suppressed myoglobin-induced expression of TLR4, NF-?B, and proinflammatory cytokine levels in macrophage RAW264.7 cells (P < 0.01). Conclusion:: The pharmacological inhibition of TLR4/NF-?B exhibited protective effects on rhabdomyolysis-induced AKI by the regulation of proinflammatory cytokine production and macrophage infiltration.