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Diffuse Lung Disease: Diffuse Lung Disease: Interstitial Lung Disease |

Exploring the Role of Curcumin Regulating PPAR-γ/PDGF-β Ignaling Pathway in the Biological Characteristics Change of Mouse Lung Fibroblasts FREE TO VIEW

Shun Liu; Ling Gong; Yi Huang; Feng Wu; Lan Pu; Lan Zhu; Wei Zhang; Chuan Huang
Author and Funding Information

The Institute of Respiratory Diseases in Zunyi City, The First People's Hospital of Zunyi City, Zunyi, China


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;149(4_S):A219. doi:10.1016/j.chest.2016.02.226
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SESSION TITLE: Diffuse Lung Disease: Interstitial Lung Disease

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE: To explore the role and mechanism of curcumin regulating peroxisome proliferater activated receptor γ (PPAR-γ) / platelet derived growth factor β (PDGF-β) signaling pathway in the biological characteristics change of mouse lung fibroblasts.

METHODS: TGFβinduced differentiation of human lung fibroblasts to myofibroblasts is a key event in the pathogenesis of pulmonary fibrosis. Curcumin inhibit fibrosis-related effects in lung fibroblasts. So we want to further explore the role and mechanism of curcumin regulating PPAR-γ/PDGF-β signaling pathway in the biological characteristics change of mouse lung fibroblasts.

RESULTS: We found that curcumin and rosiglitazone inhibit vitality of C57BL/6 in cell growth counting. And the effet of cur on C57BL/6 cell vitality was stronger than rosi. The experiment of ELISA demonstrated that the synthesis of collagen-1 increased in C57BL/6 cell with TGF-β2, but cur and rosi could inhibit the synthesis of collagen-1. The effect of cur on collagen-1 was much stronger than rosi. The experiment of immunofluorescence indicated that the expression of α-SMA increased in C57BL/6 cell with TGF-β2, but cur and rosi could inhibit the expression of α-SMA. The effect of cur on α-SMA was much stronger than rosi. The experiment of RT-PCR demonstrated that the expression of PPAR-γmRNA increased with the increasing concentration of cur and rosi, and the expression of PDGFR-β mRNA decreased with the decreasing concentration of cur and rosi. The concentration alteration of cur and rosi has nothing to do with the expression of FGFR1 mRNA. What’s more, the effect of cur on expression of PPAR-γ mRNA and PDGF-β mRNA was much stronger than rosi. In western blotting experiment, we found that rosiglitazone and curcumin up-regulate PPAR-γ protein expression level with depending rising concentration. The effect of cur on expression of PPAR-γ protein was much stronger than rosi.

CONCLUSIONS: Curcumin and rosiglitazone can inhibit the induction of TGF-β2 in alterations of biological characteristics of mouse lung fibroblasts. They include inhibition of transformation of fibroblasts, suppression of vitality of mouse lung fibroblasts, down regulation of collagen and α-SMA. Curcumin has stronger inhibition effecton proliferation and vitality of mouse lung fibroblasts than rosiglitazone. Maybe, it activatesthe PPAR-γ anddown-regulates the expression of PDGF-β. It suggests that curcumin is an emerging new anti-fibrotic drug.

CLINICAL IMPLICATIONS: These study may provide for us an emerging new anti-fibrotic drug.

DISCLOSURE: The following authors have nothing to disclose: Shun Liu, Ling Gong, Yi Huang, Feng Wu, Lan Pu, Lan Zhu, Wei Zhang, Chuan Huang

No Product/Research Disclosure Information


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