β-Cryptoxanthin alleviates diet-induced nonalcoholic steatohepatitis by suppressing inflammatory gene expression in mice
Recent nutritional epidemiological surveys showed that serum β-cryptoxanthin inversely associates with the risks for insulin resistance and liver dysfunction. Consumption of β-cryptoxanthin possibly prevents nonalcoholic steatohepatitis (NASH), which is suggested to be caused by insulin resistance a...
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| Veröffentlicht in: | PloS one 2014-05, Vol.9 (5), p.e98294 |
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| creator | Kobori, Masuko Ni, Yinhua Takahashi, Yumiko Watanabe, Natsumi Sugiura, Minoru Ogawa, Kazunori Nagashimada, Mayumi Kaneko, Shuichi Naito, Shigehiro Ota, Tsuguhito |
| description | Recent nutritional epidemiological surveys showed that serum β-cryptoxanthin inversely associates with the risks for insulin resistance and liver dysfunction. Consumption of β-cryptoxanthin possibly prevents nonalcoholic steatohepatitis (NASH), which is suggested to be caused by insulin resistance and oxidative stress from nonalcoholic fatty liver disease. To evaluate the effect of β-cryptoxanthin on diet-induced NASH, we fed a high-cholesterol and high-fat diet (CL diet) with or without 0.003% β-cryptoxanthin to C56BL/6J mice for 12 weeks. After feeding, β-cryptoxanthin attenuated fat accumulation, increases in Kupffer and activated stellate cells, and fibrosis in CL diet-induced NASH in the mice. Comprehensive gene expression analysis showed that although β-cryptoxanthin histochemically reduced steatosis, it was more effective in inhibiting inflammatory gene expression change in NASH. β-Cryptoxanthin reduced the alteration of expression of genes associated with cell death, inflammatory responses, infiltration and activation of macrophages and other leukocytes, quantity of T cells, and free radical scavenging. However, it showed little effect on the expression of genes related to cholesterol and other lipid metabolism. The expression of markers of M1 and M2 macrophages, T helper cells, and cytotoxic T cells was significantly induced in NASH and reduced by β-cryptoxanthin. β-Cryptoxanthin suppressed the expression of lipopolysaccharide (LPS)-inducible and/or TNFα-inducible genes in NASH. Increased levels of the oxidative stress marker thiobarbituric acid reactive substances (TBARS) were reduced by β-cryptoxanthin in NASH. Thus, β-cryptoxanthin suppresses inflammation and the resulting fibrosis probably by primarily suppressing the increase and activation of macrophages and other immune cells. Reducing oxidative stress is likely to be a major mechanism of inflammation and injury suppression in the livers of mice with NASH. |
| doi_str_mv | 10.1371/journal.pone.0098294 |
| format | Article |
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Consumption of β-cryptoxanthin possibly prevents nonalcoholic steatohepatitis (NASH), which is suggested to be caused by insulin resistance and oxidative stress from nonalcoholic fatty liver disease. To evaluate the effect of β-cryptoxanthin on diet-induced NASH, we fed a high-cholesterol and high-fat diet (CL diet) with or without 0.003% β-cryptoxanthin to C56BL/6J mice for 12 weeks. After feeding, β-cryptoxanthin attenuated fat accumulation, increases in Kupffer and activated stellate cells, and fibrosis in CL diet-induced NASH in the mice. Comprehensive gene expression analysis showed that although β-cryptoxanthin histochemically reduced steatosis, it was more effective in inhibiting inflammatory gene expression change in NASH. β-Cryptoxanthin reduced the alteration of expression of genes associated with cell death, inflammatory responses, infiltration and activation of macrophages and other leukocytes, quantity of T cells, and free radical scavenging. However, it showed little effect on the expression of genes related to cholesterol and other lipid metabolism. The expression of markers of M1 and M2 macrophages, T helper cells, and cytotoxic T cells was significantly induced in NASH and reduced by β-cryptoxanthin. β-Cryptoxanthin suppressed the expression of lipopolysaccharide (LPS)-inducible and/or TNFα-inducible genes in NASH. Increased levels of the oxidative stress marker thiobarbituric acid reactive substances (TBARS) were reduced by β-cryptoxanthin in NASH. Thus, β-cryptoxanthin suppresses inflammation and the resulting fibrosis probably by primarily suppressing the increase and activation of macrophages and other immune cells. Reducing oxidative stress is likely to be a major mechanism of inflammation and injury suppression in the livers of mice with NASH.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0098294</identifier><identifier>PMID: 24858832</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Alcohol ; Animals ; Antigens, Differentiation - biosynthesis ; Biology and Life Sciences ; Brain research ; Cell activation ; Cell death ; Cholesterol ; Cholesterol - adverse effects ; Cholesterol - pharmacology ; Citrus unshiu ; Cryptoxanthins - pharmacology ; Cytotoxicity ; Diabetes ; Diet ; Dietary Fats - adverse effects ; Dietary Fats - pharmacology ; Disease control ; Epidemiology ; Ethanol ; Fatty liver ; Fibrosis ; Food ; Free radicals ; Gene expression ; Gene Expression Regulation - drug effects ; Genes ; Helper cells ; Hepatology ; High cholesterol diet ; High fat diet ; Homeostasis ; Immune system ; Infiltration ; Inflammation ; Inflammation - chemically induced ; Inflammation - drug therapy ; Insulin ; Insulin Resistance ; Laboratory animals ; Leukocytes ; Lipid metabolism ; Lipids ; Lipopolysaccharides ; Liver ; Liver diseases ; Lymphocytes ; Lymphocytes T ; Macrophages ; Macrophages - metabolism ; Macrophages - pathology ; Male ; Medicine and Health Sciences ; Metabolic syndrome ; Metabolism ; Metabolites ; Mice ; Non-alcoholic Fatty Liver Disease - chemically induced ; Non-alcoholic Fatty Liver Disease - drug therapy ; Non-alcoholic Fatty Liver Disease - metabolism ; Non-alcoholic Fatty Liver Disease - pathology ; Nutrition research ; Obesity ; Oxidation resistance ; Oxidative stress ; Research and Analysis Methods ; Rodents ; Science ; Steatosis ; Stellate cells ; T-Lymphocytes - metabolism ; T-Lymphocytes - pathology ; Thiobarbituric acid ; Tumor necrosis factor-α ; University graduates ; Weight control</subject><ispartof>PloS one, 2014-05, Vol.9 (5), p.e98294</ispartof><rights>2014 Kobori 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>2014 Kobori et al 2014 Kobori et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-596d03b4e59300bcf7c93732fda8f3e790bef3c72f2a6b9f0faf28251ce5aa3c3</citedby><cites>FETCH-LOGICAL-c526t-596d03b4e59300bcf7c93732fda8f3e790bef3c72f2a6b9f0faf28251ce5aa3c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4032271/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4032271/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24858832$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Aguila, Marcia B.</contributor><creatorcontrib>Kobori, Masuko</creatorcontrib><creatorcontrib>Ni, Yinhua</creatorcontrib><creatorcontrib>Takahashi, Yumiko</creatorcontrib><creatorcontrib>Watanabe, Natsumi</creatorcontrib><creatorcontrib>Sugiura, Minoru</creatorcontrib><creatorcontrib>Ogawa, Kazunori</creatorcontrib><creatorcontrib>Nagashimada, Mayumi</creatorcontrib><creatorcontrib>Kaneko, Shuichi</creatorcontrib><creatorcontrib>Naito, Shigehiro</creatorcontrib><creatorcontrib>Ota, Tsuguhito</creatorcontrib><title>β-Cryptoxanthin alleviates diet-induced nonalcoholic steatohepatitis by suppressing inflammatory gene expression in mice</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Recent nutritional epidemiological surveys showed that serum β-cryptoxanthin inversely associates with the risks for insulin resistance and liver dysfunction. Consumption of β-cryptoxanthin possibly prevents nonalcoholic steatohepatitis (NASH), which is suggested to be caused by insulin resistance and oxidative stress from nonalcoholic fatty liver disease. To evaluate the effect of β-cryptoxanthin on diet-induced NASH, we fed a high-cholesterol and high-fat diet (CL diet) with or without 0.003% β-cryptoxanthin to C56BL/6J mice for 12 weeks. After feeding, β-cryptoxanthin attenuated fat accumulation, increases in Kupffer and activated stellate cells, and fibrosis in CL diet-induced NASH in the mice. Comprehensive gene expression analysis showed that although β-cryptoxanthin histochemically reduced steatosis, it was more effective in inhibiting inflammatory gene expression change in NASH. β-Cryptoxanthin reduced the alteration of expression of genes associated with cell death, inflammatory responses, infiltration and activation of macrophages and other leukocytes, quantity of T cells, and free radical scavenging. However, it showed little effect on the expression of genes related to cholesterol and other lipid metabolism. The expression of markers of M1 and M2 macrophages, T helper cells, and cytotoxic T cells was significantly induced in NASH and reduced by β-cryptoxanthin. β-Cryptoxanthin suppressed the expression of lipopolysaccharide (LPS)-inducible and/or TNFα-inducible genes in NASH. Increased levels of the oxidative stress marker thiobarbituric acid reactive substances (TBARS) were reduced by β-cryptoxanthin in NASH. Thus, β-cryptoxanthin suppresses inflammation and the resulting fibrosis probably by primarily suppressing the increase and activation of macrophages and other immune cells. Reducing oxidative stress is likely to be a major mechanism of inflammation and injury suppression in the livers of mice with NASH.</description><subject>Alcohol</subject><subject>Animals</subject><subject>Antigens, Differentiation - biosynthesis</subject><subject>Biology and Life Sciences</subject><subject>Brain research</subject><subject>Cell activation</subject><subject>Cell death</subject><subject>Cholesterol</subject><subject>Cholesterol - adverse effects</subject><subject>Cholesterol - pharmacology</subject><subject>Citrus unshiu</subject><subject>Cryptoxanthins - pharmacology</subject><subject>Cytotoxicity</subject><subject>Diabetes</subject><subject>Diet</subject><subject>Dietary Fats - adverse effects</subject><subject>Dietary Fats - pharmacology</subject><subject>Disease control</subject><subject>Epidemiology</subject><subject>Ethanol</subject><subject>Fatty liver</subject><subject>Fibrosis</subject><subject>Food</subject><subject>Free radicals</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Genes</subject><subject>Helper cells</subject><subject>Hepatology</subject><subject>High cholesterol diet</subject><subject>High fat diet</subject><subject>Homeostasis</subject><subject>Immune system</subject><subject>Infiltration</subject><subject>Inflammation</subject><subject>Inflammation - chemically induced</subject><subject>Inflammation - drug therapy</subject><subject>Insulin</subject><subject>Insulin Resistance</subject><subject>Laboratory animals</subject><subject>Leukocytes</subject><subject>Lipid metabolism</subject><subject>Lipids</subject><subject>Lipopolysaccharides</subject><subject>Liver</subject><subject>Liver diseases</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Macrophages</subject><subject>Macrophages - metabolism</subject><subject>Macrophages - pathology</subject><subject>Male</subject><subject>Medicine and Health Sciences</subject><subject>Metabolic syndrome</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Mice</subject><subject>Non-alcoholic Fatty Liver Disease - 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Consumption of β-cryptoxanthin possibly prevents nonalcoholic steatohepatitis (NASH), which is suggested to be caused by insulin resistance and oxidative stress from nonalcoholic fatty liver disease. To evaluate the effect of β-cryptoxanthin on diet-induced NASH, we fed a high-cholesterol and high-fat diet (CL diet) with or without 0.003% β-cryptoxanthin to C56BL/6J mice for 12 weeks. After feeding, β-cryptoxanthin attenuated fat accumulation, increases in Kupffer and activated stellate cells, and fibrosis in CL diet-induced NASH in the mice. Comprehensive gene expression analysis showed that although β-cryptoxanthin histochemically reduced steatosis, it was more effective in inhibiting inflammatory gene expression change in NASH. β-Cryptoxanthin reduced the alteration of expression of genes associated with cell death, inflammatory responses, infiltration and activation of macrophages and other leukocytes, quantity of T cells, and free radical scavenging. However, it showed little effect on the expression of genes related to cholesterol and other lipid metabolism. The expression of markers of M1 and M2 macrophages, T helper cells, and cytotoxic T cells was significantly induced in NASH and reduced by β-cryptoxanthin. β-Cryptoxanthin suppressed the expression of lipopolysaccharide (LPS)-inducible and/or TNFα-inducible genes in NASH. Increased levels of the oxidative stress marker thiobarbituric acid reactive substances (TBARS) were reduced by β-cryptoxanthin in NASH. Thus, β-cryptoxanthin suppresses inflammation and the resulting fibrosis probably by primarily suppressing the increase and activation of macrophages and other immune cells. Reducing oxidative stress is likely to be a major mechanism of inflammation and injury suppression in the livers of mice with NASH.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24858832</pmid><doi>10.1371/journal.pone.0098294</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2014-05, Vol.9 (5), p.e98294 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1528073954 |
| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Alcohol Animals Antigens, Differentiation - biosynthesis Biology and Life Sciences Brain research Cell activation Cell death Cholesterol Cholesterol - adverse effects Cholesterol - pharmacology Citrus unshiu Cryptoxanthins - pharmacology Cytotoxicity Diabetes Diet Dietary Fats - adverse effects Dietary Fats - pharmacology Disease control Epidemiology Ethanol Fatty liver Fibrosis Food Free radicals Gene expression Gene Expression Regulation - drug effects Genes Helper cells Hepatology High cholesterol diet High fat diet Homeostasis Immune system Infiltration Inflammation Inflammation - chemically induced Inflammation - drug therapy Insulin Insulin Resistance Laboratory animals Leukocytes Lipid metabolism Lipids Lipopolysaccharides Liver Liver diseases Lymphocytes Lymphocytes T Macrophages Macrophages - metabolism Macrophages - pathology Male Medicine and Health Sciences Metabolic syndrome Metabolism Metabolites Mice Non-alcoholic Fatty Liver Disease - chemically induced Non-alcoholic Fatty Liver Disease - drug therapy Non-alcoholic Fatty Liver Disease - metabolism Non-alcoholic Fatty Liver Disease - pathology Nutrition research Obesity Oxidation resistance Oxidative stress Research and Analysis Methods Rodents Science Steatosis Stellate cells T-Lymphocytes - metabolism T-Lymphocytes - pathology Thiobarbituric acid Tumor necrosis factor-α University graduates Weight control |
| title | β-Cryptoxanthin alleviates diet-induced nonalcoholic steatohepatitis by suppressing inflammatory gene expression in mice |
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