Table 2 The blockade of PI-3K/AKT, JNK or ERK signaling increases the rate of apoptosis in passaged HSC, which is partially counteracted 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’

Distributions (%) of apoptotic cells

   

0 mM

5 mM

10 mM

20 mM

Curcumin

−

7.30±0.4

    

Control

+

4.6±0.0.3*

    

Non-treatment

−

 

3.67±0.1

   

Control

+

 

3.35±0.1

   

SP

−

  

4.31±0.7

4.88±0.1

6.18±0.7

600125

+

  

3.93±0.2

4.10±0.2*

4.43±0.3*

LY

−

  

4.20±0.3

4.98±0.5

6.44±0.3

294002

+

  

3.86±0.3

4.09±0.5*

4.30±0.4*

PD

−

  

4.34±0.3

5.05±0.7

6.32±1.2

98059

+

  

3.99±0.1

4.12±0.4*

4.44±0.1*

  1. Serum-starved HSC were divided into two groups. One group was treated with curcumin (20 μM), or LY294002, or PD98059, or SP600125 at the indicated concentrations, in DMEM with FBS (10%) for 24 h. The other group was pretreated with the specific PPARγ inhibitor PD68235 (PD′) at 20 μM for 30 min prior to the addition of curcumin (20 μM), or one of the inhibitors at the indicated concentrations in the media with FBS (10%) for an additional 24 h. The rate of apoptotic cells was determined by flow cytometric analyses. Distributions (%) of apoptotic cells in the cell cycle in each group were expressed as means±s.d. (n=3). *P<0.05 versus cells only with the same inhibitor at the same concentration, without the pretreatment with the PPARγ inhibitor.
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