ABSTRACT
AIM: To investigate the mechanism of renal damage in chronic intermittent hypoxia (CIH) rat model.METHODS:The Sprague-Dawley rats were randomly divided into 2-week CIH group (2IH), 2-week simulated air control group (2C), 4-week CIH group (4IH) and 4-week simulated air control group (4C).HE staining, PAS staining and Masson staining were used for histological evaluation .Blood was collected for the measurement of superoxide dismutase (SOD).The mRNA expression of hypoxia-inducible factor-1α(HIF-1α), manganese superoxide dismutase (MnSOD), copper/zinc superoxide dismutase ( Cu/ZnSOD ) was detected by real-time PCR.RESULTS: ( 1 ) No significance difference of renal weight , body weight , and the ratio of renal weight to body weight was observed , while IH caused mor-phologic kidney damage , especially in 4IH group.Hypertrophy of epithelial cells in the kidney tubles and dilation in the glomeruli were observed under light microscope with HE and PAS staining , especially in 4IH group.Masson staining showed no significant fibrotic response in the kidney of the rats exposed to IH .(2) The SOD levels in the serum and kid-ney were decreased after CIH .Compared with the corresponding control groups , the levels of serum SOD were significantly lower in CIH groups, especially in 4IH group.The mRNA expression of Cu/ZnSOD and MnSOD in CIH groups decreased significantly as compared with control groups .The mRNA levels of HIF-1αwere significantly higher in CIH groups than those in the corresponding control groups .CONCLUSION: CIH induces abnormalities of glomeruli and convoluted tu-bules, while 4-week IH exposure has not led to fibrotic response .CIH participates in the process of renal oxidative stress damage by upregulating HIF-1αtranscription and downregulating Cu/ZnSOD and MnSOD transcription .