Rui Bai

Shanxi Medical University, Yangkü, Shanxi Sheng, China

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Publications (5)9.85 Total impact

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    ABSTRACT: Atherosclerosis is a chronic inflammatory disease. Intracellular adhesion molecule-1 (ICAM-1), vascular cellular adhesion molecule-1 (VCAM-1), and monocyte chemoattractant protein-1 (MCP-1) play important roles in inflammatory processes. P38 mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-κB signaling regulate ICAM-1, VCAM-1, and MCP-1 expression. Angiotensin (Ang) II upregulates ICAM-1, VCAM-1, and MCP-1 expression through the P38 MAPK and NF-κB pathways. Ang-(1-7) may oppose the actions of Ang II. We investigated whether Ang-(1-7) prevents Ang II-induced ICAM-1, VCAM-1, and MCP-1 expression in human umbilical vein endothelial cells (HUVECs). ICAM-1, VCAM-1, and MCP-1 expression was estimated by real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA); P38, NF-κB, and p-IκB-α expression was estimated by western blotting. Ang-(1-7) inhibited Ang II-induced ICAM-1, VCAM-1, and MCP-1 expression and secretion in HUVECs. Ang II sharply increased P38 MAPK phosphorylation, which was inhibited by pretreatment with Ang-(1-7). Moreover, Ang-(1-7) significantly inhibited Ang II-induced IκB-α phosphorylation and NF-κB P65 nuclear translocation. The MAS receptor antagonist A-779 abolished the suppressive effects of Ang-(1-7). Ang-(1-7) attenuates Ang II-induced ICAM-1, VCAM-1, and MCP-1 expression via the MAs receptor by suppressing the P38 and NF-κB pathways in HUVECs. Ang-(1-7) might delay the progression of inflammatory diseases, including atherosclerosis. © 2015 S. Karger AG, Basel.
    Cellular Physiology and Biochemistry 04/2015; 35(6):2472-2482. DOI:10.1159/000374047 · 3.55 Impact Factor
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    ABSTRACT: ATP-binding cassette transporter A1 (ABCA1) plays a crucial role in reverse cholesterol transport and anti-atherosclerosis. Liver X receptor alpha (LXRα) can stimulate cholesterol efflux through ABCA1. It has been well known that adiponectin has cardiovascular protection. In this study, we attempted to clarify the effect of adiponectin on expression of ABCA1, and explored the role of LXRα in the regulation of ABCA1 in RAW 264.7 macrophages. Our results showed that adiponectin increased ABCA1 expression at both the mRNA and protein levels in a dose-dependent and time-dependent manner. Consequently, adiponectin promoted cholesterol efflux and decreased cholesterol content in RAW 264.7 macrophages. Moreover, adiponectin up-regulated the expression of LXRα in a dose-dependent and time-dependent manner in RAW 264.7 macrophages. LXRα small interfering RNA completely abolished the promotion effects of adiponectin. In summary, adiponectin up-regulates ABCA1 expression via the LXRα pathway in RAW 264.7 macrophages. This novel insight could prove useful for developing new treatment strategies for cardiovascular diseases.
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    ABSTRACT: This study aims to explore the mechanism of globular adiponectin inhibiting vascular calcification. We established drug-induced rat vascular calcification model, globular adiponectin was given to observe the effect of globular Adiponectin on the degree of calcification. The markers of vascular calcification and apoptosis were also investigated. Meanwhile, the in vitro effect of globular Adiponectin on vascular calcification was also evaluated using primary cultured rat vascular smooth muscle cells. We found that globular adiponectin could inhibit drug-induced rat vascular calcification significantly in vivo. The apoptosis of vascular smooth muscle cells was also reduced. The possible mechanism could be the down-regulation of endoplasmic reticulum stress by globular adiponectin. Experiments in primary cultured vascular smooth muscle cells also confirmed that globular adiponectin could reduce cell apoptosis to suppress vascular calcification via inhibition of endoplasmic reticulum stress. This study confirmed that globular adiponectin could suppress vascular calcification; one of the mechanisms could be inhibition of endoplasmic reticulum stress to reduce cell apoptosis. It could provide an effective method in the therapy of vascular calcification-associated diseases.
    International journal of clinical and experimental pathology 01/2015; 8(3):2545-54. · 1.78 Impact Factor
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    ABSTRACT: Adenosine triphosphate‐binding cassette transporter A1 (ABCA1) and ABCG1 play crucial roles in reverse cholesterol transport, and have anti‐atherosclerosis effects, and liver X receptor alpha (LXRα) can stimulate cholesterol efflux through these transporters. Angiotensin (Ang)‐(1–7) can protect endothelial cells, inhibit smooth muscle cell growth, ameliorate inflammation and exert anti‐atherosclerotic effects. In the present study, we attempted to clarify the effect of Ang‐(1–7) on expression of ABCA1 and ABCG1, and explored the role of LXRα in the regulation of ABCA1 and ABCG1 in THP‐1 macrophages that had been incubated with angiotensin‐II (AngII). Ang‐(1–7) increased ABCA1 and ABCG1 expression in a concentration‐dependent manner at both the mRNA and protein levels, promoted cholesterol efflux, and decreased cholesterol content in THP‐1 macrophages treated with AngII. Furthermore, Ang‐(1–7) upregulated the expression of LXRα in a concentration‐dependent manner in these cells. LXRα small interfering RNA, as well as the Mas receptor antagonist A‐779, completely abolished these effects of Ang‐(1–7). In summary, Ang‐(1–7) upregulates ABCA1 and ABCG1 expression in THP‐1 macrophages treated with AngII through the Mas receptor, via the LXRα pathway. This novel insight into the molecular mechanism underlying Ang‐(1–7) and AngII interaction could prove useful for developing new strategies for treatment of cardiovascular diseases.
    Clinical and Experimental Pharmacology and Physiology 12/2014; 41(12). DOI:10.1111/1440-1681.12312 · 2.41 Impact Factor
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    ABSTRACT: AIM:: The aim of this study is to explore the mechanisms underlying the effects of globular adiponectin (gAd) onmyocardial ischemia/reperfusion (I/R) injury. METHODS:: An in vivo myocardial I/R model and an in vitro neonatal rat cardiomyocyte hypoxia/reoxygenation (H/R) modelsimulating I/R injuryin vivowere adopted to investigate whether and how the cardioprotective effects of gAd are mediated by the inhibition of endoplasmic reticulum (ER) stress. RESULTS:: gAd(1 μg/g, intravenously) attenuated the myocardial infarct size, myocardial enzyme activity and apoptosis in rats with I/R, and similar protection was observed in primary cultures of neonatal rat cardiomyocytes. The protective effects of gAd were associated with the suppression of ER stress,as evidenced by reversing the upregulation of GRP78, CHOP and caspase-12 that were induced by H/R and TG. In addition, gAd conferred resistance to ER stress and cardiomyocyte injury by modulating ER Ca-ATPase (SERCA) activity. Moreover, gAd further increased H/R-enhanced Akt phosphorylation. The protective effects of gAd on ER stress and SERCA activity were abolished by preincubation of rat neonatal cardiomyocytes with the PI3K inhibitor LY294002.Consistent with this finding, I/R-induced ER stress and SERCA dysfunction were also significantly ameliorated by gAd. These effects involved PI3K/Akt signaling pathway. CONCLUSIONS:: The protective effects of gAd during I/R are mediated, at least in part, by modulating SERCA activity and consequently suppressing ER stress via the activation of PI3K/Akt signaling.
    Journal of cardiovascular pharmacology 04/2013; DOI:10.1097/FJC.0b013e31829521af · 2.11 Impact Factor