Xuezhikang contributes to greater triglyceride reduction than simvastatin in hypertriglyceridemia rats by up-regulating apolipoprotein A5 via the PPARα signaling pathway
Xuezhikang (XZK), an extract of Chinese red yeast rice, is recommended as an optimal choice for patients with coronary heart disease (CHD) with markedly elevated triglyceride (TG) levels. This study was designed to compare the hypotriglyceridemic effects between XZK and simvastatin. The role of apol...
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| Veröffentlicht in: | PloS one 2017-09, Vol.12 (9), p.e0184949-e0184949 |
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| description | Xuezhikang (XZK), an extract of Chinese red yeast rice, is recommended as an optimal choice for patients with coronary heart disease (CHD) with markedly elevated triglyceride (TG) levels. This study was designed to compare the hypotriglyceridemic effects between XZK and simvastatin. The role of apolipoprotein A5 (apoA5), a key regulator of TG metabolism and a target gene of peroxisome proliferator-activated receptor α (PPARα), was to be identified in XZK-related hypotriglyceridemic actions. For these goals, hypertriglyceridemia of rats was induced by a high-fructose diet. In order to investigate the hypotriglyceridemic effects of XZK and simvastatin on these animals based on an equivalent low-density lipoprotein cholesterol (LDL-C) lowering power, we titrated their doses (XZK 80 mg/kg/d versus simvastatin 1 mg/kg/d) according to plasma LDL-C reduction of rats. Similarly, we titrated the target doses of the two agents (XZK 500 μg/ml versus simvastatin 10 μM) according to hepatocyte LDL receptor expressions, and then compared the effects of the two agents on TG and apoA5 of hepatocytes in vitro. Our results showed that XZK (80 mg/kg/d) had higher hypotriglyceridemic performance than simvastatin (1 mg/kg/d) on these animals albeit their equivalent LDL-C lowering power. Higher plasma apoA5 levels and hepatic apoA5 expressions were observed in rats treated with XZK (80 mg/kg/d) than simvastatin (1 mg/kg/d). Further, XZK (80 mg/kg/d) contributed to higher hepatic PPARα expressions of rats than simvastatin (1 mg/kg/d). Although the two agents led to an equivalent up-regulation of LDL receptors of hepatocytes, more TG reduction and apoA5 elevation were detected in hepatocytes treated with XZK (500 μg/ml) than simvastatin (10 μM). However, PPARα knockdown eliminated the above effects of XZK on hepatocytes. Therefore, our study indicates that XZK has greater hypotriglyceridemic performance than simvastatin in the setting of an equivalent LDL-C lowering power, which is attributed to more apoA5 up-regulation by this agent via the PPARα signaling pathway. |
| doi_str_mv | 10.1371/journal.pone.0184949 |
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This study was designed to compare the hypotriglyceridemic effects between XZK and simvastatin. The role of apolipoprotein A5 (apoA5), a key regulator of TG metabolism and a target gene of peroxisome proliferator-activated receptor α (PPARα), was to be identified in XZK-related hypotriglyceridemic actions. For these goals, hypertriglyceridemia of rats was induced by a high-fructose diet. In order to investigate the hypotriglyceridemic effects of XZK and simvastatin on these animals based on an equivalent low-density lipoprotein cholesterol (LDL-C) lowering power, we titrated their doses (XZK 80 mg/kg/d versus simvastatin 1 mg/kg/d) according to plasma LDL-C reduction of rats. Similarly, we titrated the target doses of the two agents (XZK 500 μg/ml versus simvastatin 10 μM) according to hepatocyte LDL receptor expressions, and then compared the effects of the two agents on TG and apoA5 of hepatocytes in vitro. Our results showed that XZK (80 mg/kg/d) had higher hypotriglyceridemic performance than simvastatin (1 mg/kg/d) on these animals albeit their equivalent LDL-C lowering power. Higher plasma apoA5 levels and hepatic apoA5 expressions were observed in rats treated with XZK (80 mg/kg/d) than simvastatin (1 mg/kg/d). Further, XZK (80 mg/kg/d) contributed to higher hepatic PPARα expressions of rats than simvastatin (1 mg/kg/d). Although the two agents led to an equivalent up-regulation of LDL receptors of hepatocytes, more TG reduction and apoA5 elevation were detected in hepatocytes treated with XZK (500 μg/ml) than simvastatin (10 μM). However, PPARα knockdown eliminated the above effects of XZK on hepatocytes. Therefore, our study indicates that XZK has greater hypotriglyceridemic performance than simvastatin in the setting of an equivalent LDL-C lowering power, which is attributed to more apoA5 up-regulation by this agent via the PPARα signaling pathway.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0184949</identifier><identifier>PMID: 28934253</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Anticholesteremic Agents - pharmacology ; Apolipoprotein A-V - genetics ; Apolipoprotein A-V - metabolism ; Apolipoproteins ; Atherosclerosis ; Biology and Life Sciences ; Cardiovascular disease ; Cardiovascular diseases ; Cells, Cultured ; Cholesterol ; Coronary artery disease ; Drinking water ; Drug dosages ; Drugs, Chinese Herbal - pharmacology ; Equivalence ; Fatty acids ; Fructose ; Gene Expression Regulation - drug effects ; Heart diseases ; Hepatocytes ; Hepatocytes - cytology ; Hepatocytes - drug effects ; Hepatocytes - metabolism ; Hypertriglyceridemia ; Hypertriglyceridemia - drug therapy ; Hypertriglyceridemia - metabolism ; Hypertriglyceridemia - pathology ; Lipid Metabolism ; Lipids ; Low density lipoprotein ; Male ; Medicine ; Medicine and Health Sciences ; Metabolism ; Peroxisome proliferator-activated receptors ; Physical Sciences ; Plasma ; PPAR alpha - genetics ; PPAR alpha - metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors ; Reduction ; Rodents ; Signal transduction ; Simvastatin ; Simvastatin - pharmacology ; Statins ; Triglycerides ; Triglycerides - metabolism ; Yeast</subject><ispartof>PloS one, 2017-09, Vol.12 (9), p.e0184949-e0184949</ispartof><rights>2017 Zhao et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2017 Zhao et al 2017 Zhao et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-e8c2b16dfeffc59619d8dbd1a25c8dd60759cd5d1f52300fb72bf2803b0f4c483</citedby><cites>FETCH-LOGICAL-c526t-e8c2b16dfeffc59619d8dbd1a25c8dd60759cd5d1f52300fb72bf2803b0f4c483</cites><orcidid>0000-0003-4988-425X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5608289/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5608289/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28934253$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Rajasingh, Johnson</contributor><creatorcontrib>Zhao, Shui-Ping</creatorcontrib><creatorcontrib>Li, Rong</creatorcontrib><creatorcontrib>Dai, Wen</creatorcontrib><creatorcontrib>Yu, Bi-Lian</creatorcontrib><creatorcontrib>Chen, Lu-Zhu</creatorcontrib><creatorcontrib>Huang, Xian-Sheng</creatorcontrib><title>Xuezhikang contributes to greater triglyceride reduction than simvastatin in hypertriglyceridemia rats by up-regulating apolipoprotein A5 via the PPARα signaling pathway</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Xuezhikang (XZK), an extract of Chinese red yeast rice, is recommended as an optimal choice for patients with coronary heart disease (CHD) with markedly elevated triglyceride (TG) levels. This study was designed to compare the hypotriglyceridemic effects between XZK and simvastatin. The role of apolipoprotein A5 (apoA5), a key regulator of TG metabolism and a target gene of peroxisome proliferator-activated receptor α (PPARα), was to be identified in XZK-related hypotriglyceridemic actions. For these goals, hypertriglyceridemia of rats was induced by a high-fructose diet. In order to investigate the hypotriglyceridemic effects of XZK and simvastatin on these animals based on an equivalent low-density lipoprotein cholesterol (LDL-C) lowering power, we titrated their doses (XZK 80 mg/kg/d versus simvastatin 1 mg/kg/d) according to plasma LDL-C reduction of rats. Similarly, we titrated the target doses of the two agents (XZK 500 μg/ml versus simvastatin 10 μM) according to hepatocyte LDL receptor expressions, and then compared the effects of the two agents on TG and apoA5 of hepatocytes in vitro. Our results showed that XZK (80 mg/kg/d) had higher hypotriglyceridemic performance than simvastatin (1 mg/kg/d) on these animals albeit their equivalent LDL-C lowering power. Higher plasma apoA5 levels and hepatic apoA5 expressions were observed in rats treated with XZK (80 mg/kg/d) than simvastatin (1 mg/kg/d). Further, XZK (80 mg/kg/d) contributed to higher hepatic PPARα expressions of rats than simvastatin (1 mg/kg/d). Although the two agents led to an equivalent up-regulation of LDL receptors of hepatocytes, more TG reduction and apoA5 elevation were detected in hepatocytes treated with XZK (500 μg/ml) than simvastatin (10 μM). However, PPARα knockdown eliminated the above effects of XZK on hepatocytes. Therefore, our study indicates that XZK has greater hypotriglyceridemic performance than simvastatin in the setting of an equivalent LDL-C lowering power, which is attributed to more apoA5 up-regulation by this agent via the PPARα signaling pathway.</description><subject>Animals</subject><subject>Anticholesteremic Agents - pharmacology</subject><subject>Apolipoprotein A-V - genetics</subject><subject>Apolipoprotein A-V - metabolism</subject><subject>Apolipoproteins</subject><subject>Atherosclerosis</subject><subject>Biology and Life Sciences</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular diseases</subject><subject>Cells, Cultured</subject><subject>Cholesterol</subject><subject>Coronary artery disease</subject><subject>Drinking water</subject><subject>Drug dosages</subject><subject>Drugs, Chinese Herbal - pharmacology</subject><subject>Equivalence</subject><subject>Fatty acids</subject><subject>Fructose</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Heart diseases</subject><subject>Hepatocytes</subject><subject>Hepatocytes - cytology</subject><subject>Hepatocytes - drug effects</subject><subject>Hepatocytes - metabolism</subject><subject>Hypertriglyceridemia</subject><subject>Hypertriglyceridemia - drug therapy</subject><subject>Hypertriglyceridemia - metabolism</subject><subject>Hypertriglyceridemia - pathology</subject><subject>Lipid Metabolism</subject><subject>Lipids</subject><subject>Low density lipoprotein</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine and Health Sciences</subject><subject>Metabolism</subject><subject>Peroxisome proliferator-activated receptors</subject><subject>Physical Sciences</subject><subject>Plasma</subject><subject>PPAR alpha - genetics</subject><subject>PPAR alpha - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors</subject><subject>Reduction</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Simvastatin</subject><subject>Simvastatin - pharmacology</subject><subject>Statins</subject><subject>Triglycerides</subject><subject>Triglycerides - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Shui-Ping</au><au>Li, Rong</au><au>Dai, Wen</au><au>Yu, Bi-Lian</au><au>Chen, Lu-Zhu</au><au>Huang, Xian-Sheng</au><au>Rajasingh, Johnson</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Xuezhikang contributes to greater triglyceride reduction than simvastatin in hypertriglyceridemia rats by up-regulating apolipoprotein A5 via the PPARα signaling pathway</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2017-09-21</date><risdate>2017</risdate><volume>12</volume><issue>9</issue><spage>e0184949</spage><epage>e0184949</epage><pages>e0184949-e0184949</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Xuezhikang (XZK), an extract of Chinese red yeast rice, is recommended as an optimal choice for patients with coronary heart disease (CHD) with markedly elevated triglyceride (TG) levels. This study was designed to compare the hypotriglyceridemic effects between XZK and simvastatin. The role of apolipoprotein A5 (apoA5), a key regulator of TG metabolism and a target gene of peroxisome proliferator-activated receptor α (PPARα), was to be identified in XZK-related hypotriglyceridemic actions. For these goals, hypertriglyceridemia of rats was induced by a high-fructose diet. In order to investigate the hypotriglyceridemic effects of XZK and simvastatin on these animals based on an equivalent low-density lipoprotein cholesterol (LDL-C) lowering power, we titrated their doses (XZK 80 mg/kg/d versus simvastatin 1 mg/kg/d) according to plasma LDL-C reduction of rats. Similarly, we titrated the target doses of the two agents (XZK 500 μg/ml versus simvastatin 10 μM) according to hepatocyte LDL receptor expressions, and then compared the effects of the two agents on TG and apoA5 of hepatocytes in vitro. Our results showed that XZK (80 mg/kg/d) had higher hypotriglyceridemic performance than simvastatin (1 mg/kg/d) on these animals albeit their equivalent LDL-C lowering power. Higher plasma apoA5 levels and hepatic apoA5 expressions were observed in rats treated with XZK (80 mg/kg/d) than simvastatin (1 mg/kg/d). Further, XZK (80 mg/kg/d) contributed to higher hepatic PPARα expressions of rats than simvastatin (1 mg/kg/d). Although the two agents led to an equivalent up-regulation of LDL receptors of hepatocytes, more TG reduction and apoA5 elevation were detected in hepatocytes treated with XZK (500 μg/ml) than simvastatin (10 μM). However, PPARα knockdown eliminated the above effects of XZK on hepatocytes. Therefore, our study indicates that XZK has greater hypotriglyceridemic performance than simvastatin in the setting of an equivalent LDL-C lowering power, which is attributed to more apoA5 up-regulation by this agent via the PPARα signaling pathway.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28934253</pmid><doi>10.1371/journal.pone.0184949</doi><orcidid>https://orcid.org/0000-0003-4988-425X</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2017-09, Vol.12 (9), p.e0184949-e0184949 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1941325745 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Animals Anticholesteremic Agents - pharmacology Apolipoprotein A-V - genetics Apolipoprotein A-V - metabolism Apolipoproteins Atherosclerosis Biology and Life Sciences Cardiovascular disease Cardiovascular diseases Cells, Cultured Cholesterol Coronary artery disease Drinking water Drug dosages Drugs, Chinese Herbal - pharmacology Equivalence Fatty acids Fructose Gene Expression Regulation - drug effects Heart diseases Hepatocytes Hepatocytes - cytology Hepatocytes - drug effects Hepatocytes - metabolism Hypertriglyceridemia Hypertriglyceridemia - drug therapy Hypertriglyceridemia - metabolism Hypertriglyceridemia - pathology Lipid Metabolism Lipids Low density lipoprotein Male Medicine Medicine and Health Sciences Metabolism Peroxisome proliferator-activated receptors Physical Sciences Plasma PPAR alpha - genetics PPAR alpha - metabolism Rats Rats, Sprague-Dawley Receptors Reduction Rodents Signal transduction Simvastatin Simvastatin - pharmacology Statins Triglycerides Triglycerides - metabolism Yeast |
| title | Xuezhikang contributes to greater triglyceride reduction than simvastatin in hypertriglyceridemia rats by up-regulating apolipoprotein A5 via the PPARα signaling pathway |
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