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10.1371/journal.pone.0192361

http://scihub22266oqcxt.onion/10.1371/journal.pone.0192361
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C5821337!5821337!29466390
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suck abstract from ncbi


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pmid29466390      PLoS+One 2018 ; 13 (2): ä
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  • The role of complement activation in rhabdomyolysis-induced acute kidney injury #MMPMID29466390
  • Huang X; Zhao W; Zhang L; Yang X; Wang L; Chen Y; Wang J; Zhang C; Wu G
  • PLoS One 2018[]; 13 (2): ä PMID29466390show ga
  • Rhabdomyolysis (RM) may cause kidney damage and results primarily in acute kidney injury (AKI). Complement is implicated in the pathogenesis of renal diseases and ischemia-reperfusion injury (IRI), but the role of complement, especially its activation pathway(s) and its effect in RM-induced AKI, is not clear. This study established a rat model of AKI induced by RM via intramuscular treatment with glycerol. Cobra venom factor (CVF) was administered via tail vein injection to deplete complement 12 h prior to intramuscular injection of glycerol. We found that the complement components, including complement 3 (C3), C1q, MBL-A, factor B(fB), C5a, C5b-9, and CD59, were significantly increased in rat kidneys after intramuscular glycerol administration. However, the levels of serum BUN and Cr, renal tubular injury scores, and the number of TUNEL-positive cells decreased significantly in the CVF+AKI group. These results suggest that complement plays an important role in RM-induced AKI and that complement depletion may improve renal function and decrease renal tissue damage by reducing the inflammatory response and apoptosis.
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