Genipin Ameliorates Carbon Tetrachloride-Induced Liver Injury in Mice via the Concomitant Inhibition of Inflammation and Induction of Autophagy
Identifieur interne : 000765 ( Pmc/Curation ); précédent : 000764; suivant : 000766Genipin Ameliorates Carbon Tetrachloride-Induced Liver Injury in Mice via the Concomitant Inhibition of Inflammation and Induction of Autophagy
Auteurs : Ya Wang [République populaire de Chine] ; Tianming Zhao [République populaire de Chine] ; You Deng [République populaire de Chine] ; Lijun Hou [République populaire de Chine] ; Xiaofei Fan [République populaire de Chine] ; Lin Lin [République populaire de Chine] ; Wei Zhao [République populaire de Chine] ; Kui Jiang [République populaire de Chine] ; Chao Sun [République populaire de Chine]Source :
- Oxidative Medicine and Cellular Longevity [ 1942-0900 ] ; 2019.
Abstract
Genipin, as the most effective ingredient of various traditional medications, encompasses antioxidative, anti-inflammatory, and antibacterial capacities. More recently, it is suggested that genipin protects against septic liver damage by restoring autophagy. The purpose of the current study was to explore the protective effect of genipin against carbon tetrachloride- (CCl4-) induced acute liver injury (ALI) and its underlying molecular machinery. Our results indicated that treatment with genipin significantly reduced CCl4-induced hepatotoxicity by ameliorating histological liver changes, decreasing the aspartate aminotransferase and alanine transaminase levels, alleviating the secretion of inflammatory cytokines, and promoting autophagic flux. Moreover, genipin effectively induced the conversion of LC3 and inhibition of p62 accumulation. The liver expressions of ATG5, ATG7, and ATG12 were significantly increased by genipin pretreatment in the ALI mice model. This protective effect may be mediated by the inhibition of mTOR and the activation of p38 MAPK signaling pathways. Meanwhile, genipin attenuated CCl4-induced inflammatory response by inhibiting the NF-
Url:
DOI: 10.1155/2019/3729051
PubMed: 31885784
PubMed Central: 6927019
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Zhao</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="I3">Tianjin Institute of Digestive Disease, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Tianjin Institute of Digestive Disease, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052</wicri:regionArea></affiliation></author><author><name sortKey="Jiang, Kui" sort="Jiang, Kui" uniqKey="Jiang K" first="Kui" 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Gastroenterology, Tianjin Medical University General Hospital Airport Hospital, East Street 6, Tianjin Airport Economic Area, Tianjin 300308, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology, Tianjin Medical University General Hospital Airport Hospital, East Street 6, Tianjin Airport Economic Area, Tianjin 300308</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">31885784</idno><idno type="pmc">6927019</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6927019</idno><idno type="RBID">PMC:6927019</idno><idno type="doi">10.1155/2019/3729051</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000765</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000765</idno><idno type="wicri:Area/Pmc/Curation">000765</idno><idno type="wicri:explorRef" wicri:stream="Pmc" 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China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology, Shanxi Academy of Medical Sciences Shanxi Bethune Hospital, Taiyuan 030032</wicri:regionArea></affiliation></author><author><name sortKey="Zhao, Tianming" sort="Zhao, Tianming" uniqKey="Zhao T" first="Tianming" last="Zhao">Tianming Zhao</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="I3">Tianjin Institute of Digestive Disease, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Tianjin Institute of Digestive Disease, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052</wicri:regionArea></affiliation></author><author><name sortKey="Deng, You" sort="Deng, You" uniqKey="Deng Y" first="You" last="Deng">You Deng</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="I3">Tianjin Institute of Digestive Disease, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Tianjin Institute of Digestive Disease, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052</wicri:regionArea></affiliation></author><author><name sortKey="Hou, Lijun" sort="Hou, Lijun" uniqKey="Hou L" first="Lijun" last="Hou">Lijun Hou</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="I3">Tianjin Institute of Digestive Disease, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Tianjin Institute of Digestive Disease, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052</wicri:regionArea></affiliation></author><author><name sortKey="Fan, Xiaofei" sort="Fan, Xiaofei" uniqKey="Fan X" first="Xiaofei" last="Fan">Xiaofei Fan</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="I3">Tianjin Institute of Digestive Disease, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Tianjin Institute of Digestive Disease, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052</wicri:regionArea></affiliation></author><author><name sortKey="Lin, Lin" sort="Lin, Lin" uniqKey="Lin L" first="Lin" last="Lin">Lin Lin</name><affiliation wicri:level="1"><nlm:aff id="I4">Department of Gastroenterology, Tianjin Medical University General Hospital Airport Hospital, East Street 6, Tianjin Airport Economic Area, Tianjin 300308, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology, Tianjin Medical University General Hospital Airport Hospital, East Street 6, Tianjin Airport Economic Area, Tianjin 300308</wicri:regionArea></affiliation></author><author><name sortKey="Zhao, Wei" sort="Zhao, Wei" uniqKey="Zhao W" first="Wei" last="Zhao">Wei Zhao</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="I3">Tianjin Institute of Digestive Disease, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Tianjin Institute of Digestive Disease, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052</wicri:regionArea></affiliation></author><author><name sortKey="Jiang, Kui" sort="Jiang, Kui" uniqKey="Jiang K" first="Kui" last="Jiang">Kui Jiang</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="I3">Tianjin Institute of Digestive Disease, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Tianjin Institute of Digestive Disease, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052</wicri:regionArea></affiliation></author><author><name sortKey="Sun, Chao" sort="Sun, Chao" uniqKey="Sun C" first="Chao" last="Sun">Chao Sun</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="I3">Tianjin Institute of Digestive Disease, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Tianjin Institute of Digestive Disease, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="I4">Department of Gastroenterology, Tianjin Medical University General Hospital Airport Hospital, East Street 6, Tianjin Airport Economic Area, Tianjin 300308, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology, Tianjin Medical University General Hospital Airport Hospital, East Street 6, Tianjin Airport Economic Area, Tianjin 300308</wicri:regionArea></affiliation></author></analytic><series><title level="j">Oxidative Medicine and Cellular Longevity</title><idno type="ISSN">1942-0900</idno><idno type="eISSN">1942-0994</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Genipin, as the most effective ingredient of various traditional medications, encompasses antioxidative, anti-inflammatory, and antibacterial capacities. More recently, it is suggested that genipin protects against septic liver damage by restoring autophagy. The purpose of the current study was to explore the protective effect of genipin against carbon tetrachloride- (CCl<sub>4</sub>-) induced acute liver injury (ALI) and its underlying molecular machinery. Our results indicated that treatment with genipin significantly reduced CCl<sub>4</sub>-induced hepatotoxicity by ameliorating histological liver changes, decreasing the aspartate aminotransferase and alanine transaminase levels, alleviating the secretion of inflammatory cytokines, and promoting autophagic flux. Moreover, genipin effectively induced the conversion of LC3 and inhibition of p62 accumulation. The liver expressions of ATG5, ATG7, and ATG12 were significantly increased by genipin pretreatment in the ALI mice model. This protective effect may be mediated by the inhibition of mTOR and the activation of p38 MAPK signaling pathways. Meanwhile, genipin attenuated CCl<sub>4</sub>-induced inflammatory response by inhibiting the NF-<italic>κ</italic>B and STAT3 signaling pathway. In addition, pretreatment with autophagy inhibitor 3-methyladenine (3-MA) or inhibition of p38 MAPK by SB203580 abolished the hepatoprotective effect of genipin. Taken together, our study implicates that genipin has a protective potential against CCl<sub>4</sub>-induced hepatotoxicity, which might be strongly associated with the induction of autophagy and the attenuation of inflammatory response.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Khoury, T" uniqKey="Khoury T">T. Khoury</name></author><author><name sortKey="Rmeileh, A A" uniqKey="Rmeileh A">A. A. Rmeileh</name></author><author><name sortKey="Yosha, L" uniqKey="Yosha L">L. Yosha</name></author><author><name sortKey="Benson, A A" uniqKey="Benson A">A. A. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Oxid Med Cell Longev</journal-id><journal-id journal-id-type="iso-abbrev">Oxid Med Cell Longev</journal-id><journal-id journal-id-type="publisher-id">OMCL</journal-id><journal-title-group><journal-title>Oxidative Medicine and Cellular Longevity</journal-title></journal-title-group><issn pub-type="ppub">1942-0900</issn><issn pub-type="epub">1942-0994</issn><publisher><publisher-name>Hindawi</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31885784</article-id><article-id pub-id-type="pmc">6927019</article-id><article-id pub-id-type="doi">10.1155/2019/3729051</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title>Genipin Ameliorates Carbon Tetrachloride-Induced Liver Injury in Mice via the Concomitant Inhibition of Inflammation and Induction of Autophagy</article-title></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0001-5375-3901</contrib-id><name><surname>Wang</surname><given-names>Ya</given-names></name><xref ref-type="aff" rid="I1"><sup>1</sup></xref><xref ref-type="aff" rid="I2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0002-4909-7160</contrib-id><name><surname>Zhao</surname><given-names>Tianming</given-names></name><xref ref-type="aff" rid="I1"><sup>1</sup></xref><xref ref-type="aff" rid="I3"><sup>3</sup></xref></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0003-0393-1153</contrib-id><name><surname>Deng</surname><given-names>You</given-names></name><xref ref-type="aff" rid="I1"><sup>1</sup></xref><xref ref-type="aff" rid="I3"><sup>3</sup></xref></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0002-7005-6937</contrib-id><name><surname>Hou</surname><given-names>Lijun</given-names></name><xref ref-type="aff" rid="I1"><sup>1</sup></xref><xref ref-type="aff" rid="I3"><sup>3</sup></xref></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0001-6273-3902</contrib-id><name><surname>Fan</surname><given-names>Xiaofei</given-names></name><xref ref-type="aff" rid="I1"><sup>1</sup></xref><xref ref-type="aff" rid="I3"><sup>3</sup></xref></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0002-2533-2103</contrib-id><name><surname>Lin</surname><given-names>Lin</given-names></name><xref ref-type="aff" rid="I4"><sup>4</sup></xref></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0001-6707-7211</contrib-id><name><surname>Zhao</surname><given-names>Wei</given-names></name><xref ref-type="aff" rid="I1"><sup>1</sup></xref><xref ref-type="aff" rid="I3"><sup>3</sup></xref></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0002-5935-1409</contrib-id><name><surname>Jiang</surname><given-names>Kui</given-names></name><email>kjiang@tmu.edu.cn</email><xref ref-type="aff" rid="I1"><sup>1</sup></xref><xref ref-type="aff" rid="I3"><sup>3</sup></xref></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0002-0380-7999</contrib-id><name><surname>Sun</surname><given-names>Chao</given-names></name><email>chaosun@tmu.edu.cn</email><xref ref-type="aff" rid="I1"><sup>1</sup></xref><xref ref-type="aff" rid="I3"><sup>3</sup></xref><xref ref-type="aff" rid="I4"><sup>4</sup></xref></contrib></contrib-group><aff id="I1"><sup>1</sup>Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052, China</aff><aff id="I2"><sup>2</sup>Department of Gastroenterology, Shanxi Academy of Medical Sciences Shanxi Bethune Hospital, Taiyuan 030032, China</aff><aff id="I3"><sup>3</sup>Tianjin Institute of Digestive Disease, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052, China</aff><aff id="I4"><sup>4</sup>Department of Gastroenterology, Tianjin Medical University General Hospital Airport Hospital, East Street 6, Tianjin Airport Economic Area, Tianjin 300308, China</aff><author-notes><fn fn-type="other"><p>Academic Editor: Giuseppe Cirillo</p></fn></author-notes><pub-date pub-type="collection"><year>2019</year></pub-date><pub-date pub-type="epub"><day>11</day><month>12</month><year>2019</year></pub-date><volume>2019</volume><elocation-id>3729051</elocation-id><history><date date-type="received"><day>2</day><month>7</month><year>2019</year></date><date date-type="rev-recd"><day>4</day><month>11</month><year>2019</year></date><date date-type="accepted"><day>7</day><month>11</month><year>2019</year></date></history><permissions><copyright-statement>Copyright © 2019 Ya Wang et al.</copyright-statement><copyright-year>2019</copyright-year><license xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p></license></permissions><abstract><p>Genipin, as the most effective ingredient of various traditional medications, encompasses antioxidative, anti-inflammatory, and antibacterial capacities. More recently, it is suggested that genipin protects against septic liver damage by restoring autophagy. The purpose of the current study was to explore the protective effect of genipin against carbon tetrachloride- (CCl<sub>4</sub>-) induced acute liver injury (ALI) and its underlying molecular machinery. Our results indicated that treatment with genipin significantly reduced CCl<sub>4</sub>-induced hepatotoxicity by ameliorating histological liver changes, decreasing the aspartate aminotransferase and alanine transaminase levels, alleviating the secretion of inflammatory cytokines, and promoting autophagic flux. Moreover, genipin effectively induced the conversion of LC3 and inhibition of p62 accumulation. The liver expressions of ATG5, ATG7, and ATG12 were significantly increased by genipin pretreatment in the ALI mice model. This protective effect may be mediated by the inhibition of mTOR and the activation of p38 MAPK signaling pathways. Meanwhile, genipin attenuated CCl<sub>4</sub>-induced inflammatory response by inhibiting the NF-<italic>κ</italic>B and STAT3 signaling pathway. In addition, pretreatment with autophagy inhibitor 3-methyladenine (3-MA) or inhibition of p38 MAPK by SB203580 abolished the hepatoprotective effect of genipin. Taken together, our study implicates that genipin has a protective potential against CCl<sub>4</sub>-induced hepatotoxicity, which might be strongly associated with the induction of autophagy and the attenuation of inflammatory response.</p></abstract><funding-group><award-group><funding-source>National Natural Science Foundation of China</funding-source><award-id>81500397</award-id></award-group></funding-group></article-meta></front><floats-group><fig id="fig1" orientation="portrait" position="float"><label>Figure 1</label><caption><p>Effects of genipin on serum ALT/AST activity (a), H&E staining (b), macroscopic examination (c), and histological score (d) at 12, 24, and 48 h after CCl<sub>4</sub> exposure. Mice were intraperitoneally injected a mixture of CCl<sub>4</sub> (50%) and oil (50%) at a dose of 2 ml·kg<sup>−1</sup> body weight. Mice received an intravenous injection of 2.5 mg·kg<sup>−1</sup> genipin 2 h before CCl<sub>4</sub> exposure. Results are presented as mean ± SEM for six mice per group. Significantly different (<sup>∗∗∗</sup><italic>p</italic> < 0.001) from the control group. Significantly different (<sup>##</sup><italic>p</italic> < 0.01 and <sup>##</sup><italic>p</italic> < 0.001) from the CCl<sub>4</sub> group.</p></caption><graphic xlink:href="OMCL2019-3729051.001"></graphic></fig><fig id="fig2" orientation="portrait" position="float"><label>Figure 2</label><caption><p>Effect of genipin and 3-MA on LC3-II, p62, ATG5, ATG7, ATG12, and Beclin-1 protein expressions (a) and transmission electron microscopy images (b) at 48 h after CCl<sub>4</sub> exposure. Mice were intraperitoneally injected a mixture of CCl<sub>4</sub> (50%) and oil (50%) at a dose of 2 ml·kg<sup>−1</sup> body weight. Mice received an intravenous injection of 2.5 mg·kg<sup>−1</sup> genipin 2 h before CCl<sub>4</sub> exposure. Mice were pretreated with 3-MA before genipin. Results are presented as mean ± SEM for each group. Significantly different (<sup>∗</sup><italic>p</italic> < 0.05, <sup>∗∗</sup><italic>p</italic> < 0.01, and <sup>∗∗∗</sup><italic>p</italic> < 0.001) from the control group. Significantly different (<sup>#</sup><italic>p</italic> < 0.05 and <sup>##</sup><italic>p</italic> < 0.01) from the CCl<sub>4</sub> group. Significantly different (<sup>&</sup><italic>p</italic> < 0.05, <sup>&&</sup><italic>p</italic> < 0.01, and <sup>&&&</sup><italic>p</italic> < 0.001) from the CCl<sub>4</sub>+genipin group.</p></caption><graphic xlink:href="OMCL2019-3729051.002"></graphic></fig><fig id="fig3" orientation="portrait" position="float"><label>Figure 3</label><caption><p>Effect of genipin and 3-MA on serum ALT activity (a), AST activity (b), H&E staining (c), and histological score (d). Mice were intraperitoneally injected a mixture of CCl<sub>4</sub> (50%) and oil (50%) at a dose of 2 ml·kg<sup>−1</sup> body weight. Mice received an intravenous injection of 2.5 mg·kg<sup>−1</sup> genipin 2 h before CCl<sub>4</sub> exposure. Mice were pretreated with 3-MA before genipin. Significantly different (<sup>∗∗∗</sup><italic>p</italic> < 0.001) from the control group. Significantly different (<sup>##</sup><italic>p</italic> < 0.01 and <sup>###</sup><italic>p</italic> < 0.001) from the CCl<sub>4</sub> group. Significantly different (<sup>&</sup><italic>p</italic> < 0.05 and <sup>&&</sup><italic>p</italic> < 0.01) from the CCl<sub>4</sub>+genipin group.</p></caption><graphic xlink:href="OMCL2019-3729051.003"></graphic></fig><fig id="fig4" orientation="portrait" position="float"><label>Figure 4</label><caption><p>Effect of genipin and/or 3-MA on mTOR (a) and p-JNK, p-p38, and p-ERK (b) protein expressions at 48 h after CCl<sub>4</sub> exposure. Mice were intraperitoneally injected a mixture of CCl<sub>4</sub> (50%) and oil (50%) at a dose of 2 ml·kg<sup>−1</sup> body weight. Mice received an intravenous injection of 2.5 mg·kg<sup>−1</sup> genipin 2 h before CCl<sub>4</sub> exposure. Mice were pretreated with 3-MA before genipin. Significantly different (<sup>∗∗</sup><italic>p</italic> < 0.01) from the control group. Significantly different (<sup>#</sup><italic>p</italic> < 0.05 and <sup>###</sup><italic>p</italic> < 0.001) from the CCl<sub>4</sub> group. Significantly different (<sup>&&</sup><italic>p</italic> < 0.01) from the CCl<sub>4</sub>+genipin group.</p></caption><graphic xlink:href="OMCL2019-3729051.004"></graphic></fig><fig id="fig5" orientation="portrait" position="float"><label>Figure 5</label><caption><p>Effect of genipin and SB203580 on serum ALT/AST activity (a), H&E staining (b), macroscopic examination (c), and LC3-II and p62 protein expressions (d). Mice were intraperitoneally injected a mixture of CCl<sub>4</sub> (50%) and oil (50%) at a dose of 2 ml·kg<sup>−1</sup> body weight. Mice received an intravenous injection of 2.5 mg·kg<sup>−1</sup> genipin 2 h before CCl<sub>4</sub> exposure. Mice were pretreated with SB203580 before genipin. Significantly different (<sup>∗∗∗</sup><italic>p</italic> < 0.001) from the control group. Significantly different (<sup>#</sup><italic>p</italic> < 0.05, <sup>##</sup><italic>p</italic> < 0.01, and <sup>###</sup><italic>p</italic> < 0.001) from the CCl<sub>4</sub> group. Significantly different (<sup>&&</sup><italic>p</italic> < 0.01 and <sup>&&&</sup><italic>p</italic> < 0.001) from the CCl<sub>4</sub>+genipin group.</p></caption><graphic xlink:href="OMCL2019-3729051.005"></graphic></fig><fig id="fig6" orientation="portrait" position="float"><label>Figure 6</label><caption><p>Effect of genipin and/or 3-MA on serum inflammatory parameters (a) and NF-<italic>κ</italic>B and p-STAT3 (b) protein expressions at 48 h after CCl<sub>4</sub> exposure. Mice were intraperitoneally injected a mixture of CCl<sub>4</sub> (50%) and oil (50%) at a dose of 2 ml·kg<sup>−1</sup> body weight. Mice received an intravenous injection of 2.5 mg·kg<sup>−1</sup> genipin 2 h before CCl<sub>4</sub> exposure. Mice were pretreated with 3-MA before genipin. Significantly different (<sup>∗</sup><italic>p</italic> < 0.05 and <sup>∗∗∗</sup><italic>p</italic> < 0.001) from the control group. Significantly different (<sup>#</sup><italic>p</italic> < 0.05 and <sup>###</sup><italic>p</italic> < 0.001) from the CCl<sub>4</sub> group. Significantly different (<sup>&</sup><italic>p</italic> < 0.05 and <sup>&&&</sup><italic>p</italic> < 0.001) from the CCl<sub>4</sub>+genipin group.</p></caption><graphic xlink:href="OMCL2019-3729051.006"></graphic></fig></floats-group></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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