Table 1 The blockade of the PI-3K/AKT, ERK and/or JNK signaling pathways results in the reduction in HSC growth, which is partially eliminated by the inhibition of PPARγ activation

From: The interruption of the PDGF and EGF signaling pathways by curcumin stimulates gene expression of PPARγ in rat activated hepatic stellate cell in vitro

 

PD′

Changes in viable cells (%)

   

0 mM

5 mM

10 mM

20 mM

Curcumin

−

75.6±5.1

    

Control

+

86.1±4.1*

    

Non-treatment

−

 

100

   

Control

+

 

103.7±2.9

   

SP

−

  

91.6±3.6

84.6±1.1

80.9±1.2

600125

+

  

93.7±1.2

91.3±0.6*

90.5±2.0*

LY

−

  

94.3±3.2

90.5±1.8

78.5±4.5

294002

+

  

97.4±10.3

94.5±3.3*

82.8±7.0*

PD

−

  

96.3±12.0

88.5±1.2

74.1±1.2

98059

+

  

98.7±9.9

93.7±4.4*

85.2±1.9*

Mixed

−

  

79.3±3.3

72.2±2.7

62±0.9

Inhibitors

+

  

84.3±1.5*

77.7±1.4*

66±3.3*

  1. Serum-starved HSC were treated with or without curcumin (20 μM), or LY294002 (LY), or PD98059 (PD), or SP600125 (SP), or a mixture of the three inhibitors at the indicated concentrations in DMEM with FBS (10%) for 24 h in the presence or absence of the PPARγ antagonist PD68235 (PD′) at 20 μM. Cell growth was analyzed by MTS assays. Results were expressed as changes in viable cells (%) (Means±s.d.) (n3), compared to the negative control with no treatment. *P<0.05 versus cells with the same specific inhibitor at the same concentration.
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