title: [Mellitin induced acute kidney injury and continuous renal replacement therapy in goat model].
abstract: OBJECTIVE
  To establish a goat model of melittin induced acute kidney injury (AKI), and to evaluate the therapeutic effect of continuous veno-venus heamofiltration (CVVH) in melittin- induced AKI.
  
  
  METHODS
  Twelve male goats were randomized into three groups: control group, melittin induced AKI group (melittin group), and CVVH intervention group (CVVH group). The AKI goat model was established by the injection of melittin via the auricular vein for four times in 48 h to reach a total dose of 0.5 mg/kg, then serum creatinine (Cr) and creatine kinase (CK) were tested every 6 h and urine output was record each hour. AKI was diagnosed when Cr level increased to the double value of control group, or the urine output decreased to less than 0. 5 mL/(kg x h) in 6 h. After the diagnosis of AKI, the animals in CVVH group received CVVH treatment for 12 h. At the end, the goats in all groups were sacrificed by anesthesia and kidney tissue samples were collected. Light microscopy and telectron microscopy observation were performed. Apoptosis was detected by immunohistochemistry and TUNEL technique.
  
  
  RESULTS
  AKI was successfully induced by melittin in the goats. The Cr level in control group was (43.95 +/- 1.59) micromol/L, while (100.75 +/- 7.87) micromol/L in AKI group and (102.10 +/- 5.06) micromol/L in CVVH group. Cr level was lowered significantly after CVVH treatment [(45.02 +/- 2.41) micromol/L in control group vs. (108.60 +/- 9.40) micromol/L in AKI group vs. (64.13 +/- 5.82) micromol/L in CVVH group, P < 0.001]. Swelling and reduction of mitochondrial crests in AKI group were more obvious than those in CVVH group. Expression of caspase-3 and apoptosis cells percentage of renal tubules in AKI group were significantly higher than those in CVVH group.
  
  
  CONCLUSIONS
  Melittin induced AKI model could be established in goats. CVVH could alleviate melittin induced AKI, probably in the mechanism to reduce the apoptosis of renal tubular cells.
authors.forename: Ying-ying
authors.initials: YY
authors.lastname: Yang
authors.forename: Ling
authors.initials: L
authors.lastname: Zhang
authors.forename: Ping
authors.initials: P
authors.lastname: Fu
authors.forename: Yi
authors.initials: Y
authors.lastname: Tang
authors.forename: Yu-liang
authors.initials: YL
authors.lastname: Zhao
authors.forename: Wei
authors.initials: W
authors.lastname: Qin
authors.forename: Fang
authors.initials: F
authors.lastname: Liu
authors.forename: Tian-lei
authors.initials: TL
authors.lastname: Cui
mesh_terms: D058186:Acute Kidney Injury / Q000139:chemically induced / Q000628:therapy*; D000818:Animals; D017209:Apoptosis; D004195:Disease Models, Animal; D006041:Goats; D007668:Kidney / Q000187:drug effects / Q000503:physiopathology; D007677:Kidney Function Tests; D008297:Male; D008555:Melitten / Q000009:adverse effects*; D017582:Renal Replacement Therapy
chemical_list: D008555:Melitten