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Emodin Inhibits Homocysteine-Induced C-Reactive Protein Generation in Vascular Smooth Muscle Cells by Regulating PPARγ Expression and ROS-ERK1/2/p38 Signal Pathway.

Pang X, Liu J, Li Y, Zhao J, Zhang X - PLoS ONE (2015)

Bottom Line: In the present study, we observed effect of emodin on Hcy-induced CRP expression in rat VSMCs and molecular mechanisms.The in vivo experiments displayed that emodin not only inhibited CRP expression in the vessel walls in mRNA and protein levels, but also reduced the circulating CRP level in hyperhomocysteinemic rats.The present study provides new evidence for the anti-inflammatory and anti-atherosclerotic effects of emodin.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, Xi'an Jiaotong University School of Medicine, Xi'an, China; Department of Clinical Pharmacy, Central Hospital of Zibo, Zibo, China.

ABSTRACT
Atherosclerosis is an inflammatory disease. As an inflammatory molecule, C-reactive protein (CRP) plays a direct role in atherogenesis. It is known that the elevated plasma homocysteine (Hcy) level is an independent risk factor for atherosclerosis. We previously reported that Hcy produces a pro-inflammatory effect by inducing CRP expression in vascular smooth muscle cells (VSMCs). In the present study, we observed effect of emodin on Hcy-induced CRP expression in rat VSMCs and molecular mechanisms. The in vitro results showed that pretreatment of VSMCs with emodin inhibited Hcy-induced mRNA and protein expression of CRP in a concentration-dependent manner. The in vivo experiments displayed that emodin not only inhibited CRP expression in the vessel walls in mRNA and protein levels, but also reduced the circulating CRP level in hyperhomocysteinemic rats. Further study revealed that emodin diminished Hcy-stimulated generation of reactive oxygen species (ROS), attenuated Hcy-activated phosphorylation of ERK1/2 and p38, and upregulated Hcy-inhibited expression of peroxisome proliferator-activated receptor gamma (PPARγ) in VSMCs. These demonstrate that emodin is able to inhibit Hcy-induced CRP generation in VSMCs, which is related to interfering with ROS-ERK1/2/p38 signal pathway and upregulating PPARγ expression. The present study provides new evidence for the anti-inflammatory and anti-atherosclerotic effects of emodin.

No MeSH data available.


Related in: MedlinePlus

Effect of emodin on the viability of VSMCs.The cells were incubated with the different concentrations of emodin for 24 h. Then, the cell viability was assayed by the MTT method. DMSO (0.1%) was used as solvent control. Results from three independent experiments were expressed as mean ± S.E.M. *P < 0.05 vs. DMSO.
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pone.0131295.g001: Effect of emodin on the viability of VSMCs.The cells were incubated with the different concentrations of emodin for 24 h. Then, the cell viability was assayed by the MTT method. DMSO (0.1%) was used as solvent control. Results from three independent experiments were expressed as mean ± S.E.M. *P < 0.05 vs. DMSO.

Mentions: In order to choose the proper concentrations of emodin used for the in vitro study, effect of emodin on the viability of VSMCs was observed. Fig 1 displays that incubation of the cells for 24 h with emodin at 0.1 μM to 10 μM hardly affected the viability of VSMCs. But, 100 μM emodin significantly decreased the cell viability by 53.5% (P < 0.05 vs. DMSO). Therefore, 0.1, 1, 10 μM of emodin were used for the in vitro study.


Emodin Inhibits Homocysteine-Induced C-Reactive Protein Generation in Vascular Smooth Muscle Cells by Regulating PPARγ Expression and ROS-ERK1/2/p38 Signal Pathway.

Pang X, Liu J, Li Y, Zhao J, Zhang X - PLoS ONE (2015)

Effect of emodin on the viability of VSMCs.The cells were incubated with the different concentrations of emodin for 24 h. Then, the cell viability was assayed by the MTT method. DMSO (0.1%) was used as solvent control. Results from three independent experiments were expressed as mean ± S.E.M. *P < 0.05 vs. DMSO.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4488440&req=5

pone.0131295.g001: Effect of emodin on the viability of VSMCs.The cells were incubated with the different concentrations of emodin for 24 h. Then, the cell viability was assayed by the MTT method. DMSO (0.1%) was used as solvent control. Results from three independent experiments were expressed as mean ± S.E.M. *P < 0.05 vs. DMSO.
Mentions: In order to choose the proper concentrations of emodin used for the in vitro study, effect of emodin on the viability of VSMCs was observed. Fig 1 displays that incubation of the cells for 24 h with emodin at 0.1 μM to 10 μM hardly affected the viability of VSMCs. But, 100 μM emodin significantly decreased the cell viability by 53.5% (P < 0.05 vs. DMSO). Therefore, 0.1, 1, 10 μM of emodin were used for the in vitro study.

Bottom Line: In the present study, we observed effect of emodin on Hcy-induced CRP expression in rat VSMCs and molecular mechanisms.The in vivo experiments displayed that emodin not only inhibited CRP expression in the vessel walls in mRNA and protein levels, but also reduced the circulating CRP level in hyperhomocysteinemic rats.The present study provides new evidence for the anti-inflammatory and anti-atherosclerotic effects of emodin.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, Xi'an Jiaotong University School of Medicine, Xi'an, China; Department of Clinical Pharmacy, Central Hospital of Zibo, Zibo, China.

ABSTRACT
Atherosclerosis is an inflammatory disease. As an inflammatory molecule, C-reactive protein (CRP) plays a direct role in atherogenesis. It is known that the elevated plasma homocysteine (Hcy) level is an independent risk factor for atherosclerosis. We previously reported that Hcy produces a pro-inflammatory effect by inducing CRP expression in vascular smooth muscle cells (VSMCs). In the present study, we observed effect of emodin on Hcy-induced CRP expression in rat VSMCs and molecular mechanisms. The in vitro results showed that pretreatment of VSMCs with emodin inhibited Hcy-induced mRNA and protein expression of CRP in a concentration-dependent manner. The in vivo experiments displayed that emodin not only inhibited CRP expression in the vessel walls in mRNA and protein levels, but also reduced the circulating CRP level in hyperhomocysteinemic rats. Further study revealed that emodin diminished Hcy-stimulated generation of reactive oxygen species (ROS), attenuated Hcy-activated phosphorylation of ERK1/2 and p38, and upregulated Hcy-inhibited expression of peroxisome proliferator-activated receptor gamma (PPARγ) in VSMCs. These demonstrate that emodin is able to inhibit Hcy-induced CRP generation in VSMCs, which is related to interfering with ROS-ERK1/2/p38 signal pathway and upregulating PPARγ expression. The present study provides new evidence for the anti-inflammatory and anti-atherosclerotic effects of emodin.

No MeSH data available.


Related in: MedlinePlus