Objective      To investigate the effects of uncoupling protein 2 (UCP2) on cardiomyocyte hypertrophy induced by indoxyl sulfate (IS).       Methods      Neonatal rat cardiomyocytes were separately treated with IS of 0

100

250

500

and 1 000 μmol/L for 1 h or with 500 μmol/L IS for 0

15

30

45

and 60 min. Then UCP2 expression was tested with Western blotting. After neonatal rat cardiomyocytes were infected with lentivirus

we observed the expressio

n of UCP2 by Western blotting and detected reactive oxygen species (ROS) production by Mitosox

TM

. Cell size was tested by immunofluorescent staining of α-actinin. ANF

BNP and β-MHC mRNA and [

3

H

]

leucine incorporation were examined as indicators of cardiomyocyte hypertrophy.       Results      Compared with the control group

IS treatment reduced the expression of UCP2 in a dose- and time-dependent manner (P0.05). UCP2 overexpression significantly suppressed ROS generation

inhibited the increase of cell volume and [

3

H

]

leucine incorporation

and reduced the mRNA expression of ANF

BNP

and β-MHC induced by IS (P0.05).       Conclusion      IS may induce cardiomyocyte hypertrophy by down-regulating UCP2 expression and enhancing oxidative stress. UCP2 overexpression may antagonize IS-induced cardiomyocyte hypertrophy by inhibiting oxidative stress.