Objective      To investigate the function and mechanism of indoxyl sulfate (IS) in inducing cardiac hypertrophy.        Methods      Rat neonatal cardiac myocytes (RNCMs) were isolated and treated with IS (100

250

500 and 1 000 μmol/L) for 3 h before using fluorescence probe 2

7-dichlorofluorescin dictate (DCFH-DA) to detect the variation of production of intracellular reactive oxygen species (ROS). RNCMs were incubated with IS (500 μmol/L) for 24 h

and then real-time PCR was applied to dete

rmine the expression of atrial natriuretic peptide (ANF)

B-type natriuretic peptide (BNP) and beta-myosin heavy chain (β-MHC) mRNA. The cardiomyocytes were treated with IS (500 μmol/L) for 48 h

3

H-leucine incorporation assay and immunocytochemical technique were adopted to measure protein synthesis rate and to mark α-smooth muscle actin (α-actinin) to observe morphology of RNCMs separately.        Results      IS caused a dose-dependent increase of ROS synthesis (P0.05)

and the expression levels of ANF

BNP and β-MHC mRNA were enhanced as well. IS (500 μmol /L) also exerted its function in increasing protein synthesis rate (P0.05) and cell area in RNCMs.        Conclusion      IS can induce hypertrophy in cardiomyocytes

probably through the enhancement of oxidative stress.