Research: PCSK9/LDLR Pathway Mediates Curcumin Trinicotinate Promoting Lipid Uptake of HepG2

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Research: PCSK9/LDLR Pathway Mediates Curcumin Trinicotinate Promoting Lipid Uptake of HepG2
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Affiliation:College of pharmacy and Biological Sciences, University of South China, Hengyang 421001, China,Division of Stem Cell Regulation and Application,State Key Laboratory of Chinese Medicine Powder and Medicine Innovation in Hunan(incubation), Hunan University of Chinese Medicine,Division of Stem Cell Regulation and Application,State Key Laboratory of Chinese Medicine Powder and Medicine Innovation in Hunan(incubation), Hunan University of Chinese Medicine;Sino-Luxembourg Cooperative Research Centre for Chinese Medicine,College of pharmacy and Biological Sciences, University of South China,Division of Stem Cell Regulation and Application,State Key Laboratory of Chinese Medicine Powder and Medicine Innovation in Hunan(incubation), Hunan University of Chinese Medicine,College of pharmacy and Biological Sciences, University of South China,Division of Stem Cell Regulation and Application,State Key Laboratory of Chinese Medicine Powder and Medicine Innovation in Hunan(incubation), Hunan University of Chinese Medicine,College of pharmacy and Biological Sciences, University of South China,Division of Stem Cell Regulation and Application,State Key Laboratory of Chinese Medicine Powder and Medicine Innovation in Hunan(incubation), Hunan University of Chinese Medicine;Sino-Luxembourg Cooperative Research Centre for Chinese Medicine
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Fund Project:This work was supported by grants from The National Natural Science Foundation of China (31371161, 81173047), Natural Science Foundation of Hunan Province (2015JJ6077, 2014JJ1024), The Construct Program of the Pharmaceutical Science Key Discipline in Hunan Province and the Innovation Team in University of South China

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Abstract:

Low-density lipoprotein cholesterol (LDL-C) is a major risk factor for the atherosclerotic cardiovascular disease (ASCVD). Over 70% of circulating LDL-C is metabolized by binding hepatic LDL receptor (LDLR). Therefore, elevation of LDLR expression would reduce the progression of ASVCD. In order to study the molecular mechanism of Curcumin Nieotinate (CurTn) reducing lipid deposition of arterial intima by lowering plasma LDL-C, HepG2 cells were treated with 5, 10, 15 μmol/L CurTn co-incubated with 25 mg/L LDL for 24 h. Cellular lipid was detected by oil red O staining. Cholesterol content was detected by cholesterol quantitative fluorometric kit. LDL uptake was visualized by DiI-LDL and Hoechst33342. The mRNA expression of LDLR and SREBP2 was analyzed by quantitative Real-time PCR (RT-Q-PCR) and protein expression of LDLR, SREBP2 and PCSK9 by Western blotting. Oil Red O staining showed that lipid droplets increased significantly in 10, 15 μmol/L CurTn groups. The content of Cholesterol and DiI-LDL uptake were higher in 10, 15 μmol/L CurTn groups than in control group. RT-Q-PCR and Western blotting showed that CurTn increased LDLR protein expression and decreased PCSK9 protein expression, although CurTn also increased SREBP2 mRNA expression. CurTn had no effect on LDLR mRNA expression in HepG2 cells. These results suggest that PCSK9/LDLR pathway may play a key role in lowering serum LDL-C and attenuating ASCVD risk by CurTn.

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ZHANG Cai-Ping, SUN Shao-Wei, GONG Yong-Zhen, OU Lu, LIN Li-Mei, ZHENG Xi, TUO Qin-Hui, LEI Xiao-Yong, LIAO Duan-Fang.Research: PCSK9/LDLR Pathway Mediates Curcumin Trinicotinate Promoting Lipid Uptake of HepG2[J]. Progress in Biochemistry and Biophysics,2015,42(9):825-832

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Received:April 23,2015
Revised:June 30,2015
Accepted:July 03,2015
Online: September 22,2015
Published: September 20,2015

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