The Expression Of PPERγ Receptor And Its Role In Renal Tubular Epithelial Cells Injury Induced By Hypoxia

OBJECTIVE Detecting the expressions of PPAR and TGF-β1in therenal tubular epithelial cell (RTEC) injury which was induced by hypoxia，tostudy the effect of rosiglitazone and GW9662treatment.METHOD Rat proximal tubular epithelial cellline NRK-52E wascultured using mixture medium of fetal bovine serum and double-antibody (94ml medium plus5ml fetal calf serum and1ml double-antibody)and was keptin the37℃50ml/L CO2incubator. After four times cell propagation,NRK-52E were randomly divided into4groups: normal group, hypoxia modelgroup, rosiglitazone intervention group and GW9662group. The normal groupwasn’t disposed. The hypoxia model group, rosiglitazone intervention groupand GW9662group group were put into vacuum tank, used a vacuum pump toremove the air from the tank, then filled it with hypoxic gas (950ml/L nitrogenand50ml/L carbon dioxide, repeated five times) to construct RTEC hypoxiainjury model. After36hours, inverted microscope were used to observe the cellmorphology change,real-time PCR were used for the detection of PPARγ andtransforming growth factor-β1(TGF-β1) mRNA expressions, and western-blotwas used for the detection of PPARγ and TGF-β1protein expressions. RESULTS1.In the hypoxia model group，cell atrophied and cell gapwidened, suggested that cell damage，Compared with hypoxia model group, thecell damage of rosiglitazone intervention group was aggravated, he cell damageof GW9662intervention group was mitigated.2. Compared with normalgroup, the mRNA and protein expressions of PPARγ in the hypoxia modelgroup, rosiglitazone intervention group and GW9662intervention group wereincreased remarkably (P<0.05); Compared with hypoxia model group, themRNA and protein expressions of PPARγ in the rosiglitazone interventiongroup were increased remarkably (P<0.05), the mRNA and protein expressionsof PPARγ in the GW9662group were decreased significantly (P<0.05).3.Compared with normal group, the mRNA and protein expressions of TGF-β1in the hypoxia model group, rosiglitazone intervention group and GW9662group were increased remarkably (P<0.05); Compared with hypoxia modelgroup, the mRNA and protein expressions of TGF-β1in the rosiglitazoneintervention group and GW9662group were decreased remarkably (P<0.05),the mRNA and protein expressions of TGF-β1in the GW9662group wereincreased significantly (P<0.05).4. Correlation analysis: The proteinexpression of PPARγ was negatively correlated with the protein expression ofTGF-β1in hypoxia model group (P <0.05).CONCLUSION The PPARγ receptor might be involved in the renaltubular epithelial cell injury induced by hypoxia. The PPARγ receptor agonistrosiglitazone may alleviate the renal tubular epithelial cell injury by increasing theexpression of PPARγ.