Kinin B_2 receptor does not exert renoprotective effects on mice with glycerol-induced rhabdomyolysis

AIM： To investigate a potential protective role of the kinin B2 receptor in a glycerol-induced rhabdomyolysis mouse model. METHODS： We separated 28 C57Bl/6 male mice into 4 groups： untreated WT animals, untreated B2 knockout mice, glycerol-treated WT and glycerol-treated B2 knockout mice. Glycerol-treated animals received one intramuscular injections of glycerol solution （50% v/v, 7 mL/kg）. After 48 h, urine and blood samples were collected to measure creatinine and urea levels. Addi-tionally, kidney samples were extracted for histological evaluation, and the mRNA expression levels of kinin B1 and B2 receptors and infammatory mediators were measured by real-time polymerase chain reaction. RESULTS： Serum creatinine and urea levels showed differences between untreated wild-type and glycerol-treated wild-type mice （0.66 ± 0.04 vs 2.61 ± 0.53 mg/dL, P 〈 0.01; and 33.51 ± 2.08 vs 330.2 ± 77.7 mg/dL, P 〈 0.005）, and between untreated B2 knock-out mice and glycerol-treated knockout mice （0.56 ± 0.03 vs 2.23 ± 0.87 mg/dL, P 〈 0.05; and 42.49 ± 3.2 vs 327.2 ± 58.4 mg/dL, P 〈 0.01）, but there was no difference between the glycerol-treated wild-type and glycerol-treated knockout mice. Glycerol was able to in-duce a striking increase in kinin B2 receptor expression （〉 30 times, 31.34 ± 8.9） in kidney. Animals injected with glycerol had a higher degree of tubular injury than untreated animals. Wild-type and knockout mice treat-ed with glycerol intramuscularly present kidney injury, with impairment in renal function. However, B2 knock-out mice treated with glycerol did not show a different phenotype regarding kidney injury markers, when com-pared to the wild-type glycerol-treated group. CONCLUSION： We conclude that the kinin B2 receptordoes not have a protective role in renal injury.

AIM:To investigate a potential protective role of the kinin B2receptor in a glycerol-induced rhabdomyolysis mouse model.METHODS:We separated 28 C57Bl/6 male mice into4 groups:untreated WT animals,untreated B2knockout mice,glycerol-treated WT and glycerol-treated B2knockout mice.Glycerol-treated animals received one intramuscular injections of glycerol solution(50%v/v,7 m L/kg).After 48 h,urine and blood samples were collected to measure creatinine and urea levels.Additionally,kidney samples were extracted for histological evaluation,and the m RNA expression levels of kinin B1 and B2 receptors and inflammatory mediators were measured by real-time polymerase chain reaction.RESULTS:Serum creatinine and urea levels showed differences between untreated wild-type and glyceroltreated wild-type mice(0.66±0.04 vs 2.61±0.53mg/d L,P<0.01;and 33.51±2.08 vs 330.2±77.7mg/d L,P<0.005),and between untreated B2knockout mice and glycerol-treated knockout mice(0.56±0.03 vs 2.23±0.87 mg/d L,P<0.05;and 42.49±3.2vs 327.2±58.4 mg/d L,P<0.01),but there was no difference between the glycerol-treated wild-type and glycerol-treated knockout mice.Glycerol was able to induce a striking increase in kinin B2receptor expression(>30 times,31.34±8.9)in kidney.Animals injected with glycerol had a higher degree of tubular injury than untreated animals.Wild-type and knockout mice treated with glycerol intramuscularly present kidney injury,with impairment in renal function.However,B2knockout mice treated with glycerol did not show a different phenotype regarding kidney injury markers,when compared to the wild-type glycerol-treated group.CONCLUSION:We conclude that the kinin B2receptordoes not have a protective role in renal injury.