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Objective: Overtraining can cause kidney damage, no effective clinical prevention measures , and how to further understanding of its pathogenesis , explore its prevention and control measures is an important issue currently facing . In this study, using rats swimming to exhaustion overtraining induced acute kidney injury animal model of overtraining is established between different times of cell adhesion molecule -1 (ICAM-1), cadherin (E-Cadherin), β - calcium catenin ( β -Catenin ) , the expression of endothelin (ET) , and renal function and renal pathology ; observed scopolamine on the above indicators , to explore adhesion molecules , endothelin -induced acute kidney injury overtraining played the role , and to deepen their understanding of the pathogenesis of , and provide experimental evidence for its prevention and control . Methods: 42 healthy male Wistar rats , weighing 200 - 220g . Randomly divided into normal control group (N ) 6 , immediately after exhaustive exercise group (S0 group ) , six hours after exhaustive exercise group (S6 group ) , 12 hours after exhaustive exercise group (S12 group ) , exhaustive 24 hours after the exercise group (S24 group ) 6 , East scopolamine 6h , 24h (D6 , D24 group ) of 6 . Exhaustive exercise each group of rats swimming to exhaustion establish overtraining cause acute kidney injury model ( single exhaustive , does not add weight ) . Scopolamine group are press 5mg/Kg intraperitoneal injection administered before exercise . All rats free access to water and standard rodent feed intake . Normal control group , exhaustive exercise 6h , 12h , 24h , scopolamine rats after exhaustive exercise instantly drying surface carrying water placed in metabolic cages and urine collected at various time intervals , urine r - glutamyl transferase ( r - GT) . Each group were sacrificing blood specimens detect serum creatinine ( Scr ) , blood urea nitrogen (BUN), creatine phosphate in muscle enzymes
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