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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.
PLoS One. 2015; 10(7):e0131295.Plos

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.

Authors+Show Affiliations

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

Pub Type(s)

Journal Article

Language

eng

PubMed ID

26131983

Citation

Pang, Xiaoming, et al. "Emodin Inhibits Homocysteine-Induced C-Reactive Protein Generation in Vascular Smooth Muscle Cells By Regulating PPARγ Expression and ROS-ERK1/2/p38 Signal Pathway." PloS One, vol. 10, no. 7, 2015, pp. e0131295.
Pang X, Liu J, Li Y, et al. Emodin Inhibits Homocysteine-Induced C-Reactive Protein Generation in Vascular Smooth Muscle Cells by Regulating PPARγ Expression and ROS-ERK1/2/p38 Signal Pathway. PLoS ONE. 2015;10(7):e0131295.
Pang, X., Liu, J., Li, Y., Zhao, J., & Zhang, X. (2015). Emodin Inhibits Homocysteine-Induced C-Reactive Protein Generation in Vascular Smooth Muscle Cells by Regulating PPARγ Expression and ROS-ERK1/2/p38 Signal Pathway. PloS One, 10(7), e0131295. https://doi.org/10.1371/journal.pone.0131295
Pang X, et al. Emodin Inhibits Homocysteine-Induced C-Reactive Protein Generation in Vascular Smooth Muscle Cells By Regulating PPARγ Expression and ROS-ERK1/2/p38 Signal Pathway. PLoS ONE. 2015;10(7):e0131295. PubMed PMID: 26131983.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Emodin Inhibits Homocysteine-Induced C-Reactive Protein Generation in Vascular Smooth Muscle Cells by Regulating PPARγ Expression and ROS-ERK1/2/p38 Signal Pathway. AU - Pang,Xiaoming, AU - Liu,Juntian, AU - Li,Yuxia, AU - Zhao,Jingjing, AU - Zhang,Xiaolu, Y1 - 2015/07/01/ PY - 2015/01/29/received PY - 2015/06/01/accepted PY - 2015/7/2/entrez PY - 2015/7/2/pubmed PY - 2016/4/9/medline SP - e0131295 EP - e0131295 JF - PloS one JO - PLoS ONE VL - 10 IS - 7 N2 - 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. SN - 1932-6203 UR - https://www.unboundmedicine.com/medline/citation/26131983/Emodin_Inhibits_Homocysteine_Induced_C_Reactive_Protein_Generation_in_Vascular_Smooth_Muscle_Cells_by_Regulating_PPARγ_Expression_and_ROS_ERK1/2/p38_Signal_Pathway_ L2 - http://dx.plos.org/10.1371/journal.pone.0131295 DB - PRIME DP - Unbound Medicine ER -