Exploration of the Components and Pharmacological Mechanisms of Keyin Pill-Induced Liver Injury Based on Network Pharmacology
Background. Keyin pill (KP), a patented medicine in China, is used to treat psoriasis. However, KP has been reported to have liver toxicity, but its toxic substance basis and underlying mechanisms remain unclear. Therefore, this study aimed to explore the pharmacological mechanisms and components of...
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description | Background. Keyin pill (KP), a patented medicine in China, is used to treat psoriasis. However, KP has been reported to have liver toxicity, but its toxic substance basis and underlying mechanisms remain unclear. Therefore, this study aimed to explore the pharmacological mechanisms and components of KP-induced liver injury through animal experiments, UPLC-QTOF/MS combined with network pharmacology. Methods. Firstly, based on the immune stress mouse model, liver function parameters and hematoxylin-eosin (H&E) staining were detected to investigate KP-induced liver injury. The UPLC-QTOF/MS method was used to identify the components of KP. CTD database and literature mining were further applied to screen nonliver protective components. Subsequently, the nonliver protective components and their corresponding targets and targets of hepatotoxicity were analyzed by the method of network pharmacology. Finally, key targets from networked pharmacology were examined by the enzyme-linked immunosorbent assay (ELISA) and molecular docking. Results. Our results indicated that KP had hepatotoxicity in male Kunming mice, which could favor hepatocyte necrosis and infiltration of inflammatory cells. A total of 70 nonliver protective compounds were identified and screened. The results of network pharmacology illustrated that methoxsalen, obacunone, limonin, and dictamnine might be the main compounds that caused liver damage. The potential hepatotoxicity mechanisms of KP might be through the IL17 and apoptosis pathways to regulate IL6, TNFα, CASP3, and CASP8 targets, thereby causing inflammation, excessive release of factors, and hepatocyte necrosis. The results of the ELISA experiments indicated that KP could increase the release of IL6 and TNFα inflammatory factors in liver tissues. Molecular docking suggested that methoxsalen, obacunone, limonin, and dictamnine had moderate binding ability with CASP3 and CASP8. Conclusion. In this study, the material basis and potential pharmacological mechanisms of KP-induced liver injury were preliminarily explored. Our research provides the initial theoretical basis for reducing the toxicity of KP. |
doi_str_mv | 10.1155/2022/9916949 |
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Keyin pill (KP), a patented medicine in China, is used to treat psoriasis. However, KP has been reported to have liver toxicity, but its toxic substance basis and underlying mechanisms remain unclear. Therefore, this study aimed to explore the pharmacological mechanisms and components of KP-induced liver injury through animal experiments, UPLC-QTOF/MS combined with network pharmacology. Methods. Firstly, based on the immune stress mouse model, liver function parameters and hematoxylin-eosin (H&E) staining were detected to investigate KP-induced liver injury. The UPLC-QTOF/MS method was used to identify the components of KP. CTD database and literature mining were further applied to screen nonliver protective components. Subsequently, the nonliver protective components and their corresponding targets and targets of hepatotoxicity were analyzed by the method of network pharmacology. Finally, key targets from networked pharmacology were examined by the enzyme-linked immunosorbent assay (ELISA) and molecular docking. Results. Our results indicated that KP had hepatotoxicity in male Kunming mice, which could favor hepatocyte necrosis and infiltration of inflammatory cells. A total of 70 nonliver protective compounds were identified and screened. The results of network pharmacology illustrated that methoxsalen, obacunone, limonin, and dictamnine might be the main compounds that caused liver damage. The potential hepatotoxicity mechanisms of KP might be through the IL17 and apoptosis pathways to regulate IL6, TNFα, CASP3, and CASP8 targets, thereby causing inflammation, excessive release of factors, and hepatocyte necrosis. The results of the ELISA experiments indicated that KP could increase the release of IL6 and TNFα inflammatory factors in liver tissues. Molecular docking suggested that methoxsalen, obacunone, limonin, and dictamnine had moderate binding ability with CASP3 and CASP8. Conclusion. In this study, the material basis and potential pharmacological mechanisms of KP-induced liver injury were preliminarily explored. Our research provides the initial theoretical basis for reducing the toxicity of KP.</description><identifier>ISSN: 1741-427X</identifier><identifier>EISSN: 1741-4288</identifier><identifier>DOI: 10.1155/2022/9916949</identifier><identifier>PMID: 36518852</identifier><language>eng</language><publisher>United States: Hindawi</publisher><subject>Animal research ; Apoptosis ; Chinese medicine ; Drug dosages ; Enzyme-linked immunosorbent assay ; Hepatotoxicity ; Inflammation ; Interleukin 17 ; Laboratory animals ; Liver ; Metabolism ; Methoxsalen ; Pharmacology ; Psoriasis ; Software ; Toxicity ; Tumor necrosis factor-α</subject><ispartof>Evidence-based complementary and alternative medicine, 2022, Vol.2022, p.9916949-14</ispartof><rights>Copyright © 2022 Bo Xing et al.</rights><rights>Copyright © 2022 Bo Xing et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2022 Bo Xing et al. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c405t-651d9eb124f21e0826e42ca06de538d280efb7c2c53a6ad5eaaf3aaadac1af893</cites><orcidid>0000-0002-9168-7316 ; 0000-0003-2011-274X ; 0000-0001-9963-9100 ; 0000-0002-8561-6810 ; 0000-0003-0381-9794 ; 0000-0002-0840-3096 ; 0000-0001-6295-4887 ; 0000-0001-9256-9971 ; 0000-0001-8246-7058 ; 0000-0003-2386-2570</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/PMC9744617/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9744617/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4010,27900,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36518852$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Zhu, Guoqi</contributor><contributor>Guoqi Zhu</contributor><creatorcontrib>Xing, Bo</creatorcontrib><creatorcontrib>Cui, Yaling</creatorcontrib><creatorcontrib>Chen, Ying</creatorcontrib><creatorcontrib>Lai, Lingyun</creatorcontrib><creatorcontrib>Zhang, Meiling</creatorcontrib><creatorcontrib>Xu, Xiangbo</creatorcontrib><creatorcontrib>Wang, Nan</creatorcontrib><creatorcontrib>Jiang, Xiaowen</creatorcontrib><creatorcontrib>Xu, Zihua</creatorcontrib><creatorcontrib>Zhao, Qingchun</creatorcontrib><title>Exploration of the Components and Pharmacological Mechanisms of Keyin Pill-Induced Liver Injury Based on Network Pharmacology</title><title>Evidence-based complementary and alternative medicine</title><addtitle>Evid Based Complement Alternat Med</addtitle><description>Background. Keyin pill (KP), a patented medicine in China, is used to treat psoriasis. However, KP has been reported to have liver toxicity, but its toxic substance basis and underlying mechanisms remain unclear. Therefore, this study aimed to explore the pharmacological mechanisms and components of KP-induced liver injury through animal experiments, UPLC-QTOF/MS combined with network pharmacology. Methods. Firstly, based on the immune stress mouse model, liver function parameters and hematoxylin-eosin (H&E) staining were detected to investigate KP-induced liver injury. The UPLC-QTOF/MS method was used to identify the components of KP. CTD database and literature mining were further applied to screen nonliver protective components. Subsequently, the nonliver protective components and their corresponding targets and targets of hepatotoxicity were analyzed by the method of network pharmacology. Finally, key targets from networked pharmacology were examined by the enzyme-linked immunosorbent assay (ELISA) and molecular docking. Results. Our results indicated that KP had hepatotoxicity in male Kunming mice, which could favor hepatocyte necrosis and infiltration of inflammatory cells. A total of 70 nonliver protective compounds were identified and screened. The results of network pharmacology illustrated that methoxsalen, obacunone, limonin, and dictamnine might be the main compounds that caused liver damage. The potential hepatotoxicity mechanisms of KP might be through the IL17 and apoptosis pathways to regulate IL6, TNFα, CASP3, and CASP8 targets, thereby causing inflammation, excessive release of factors, and hepatocyte necrosis. The results of the ELISA experiments indicated that KP could increase the release of IL6 and TNFα inflammatory factors in liver tissues. Molecular docking suggested that methoxsalen, obacunone, limonin, and dictamnine had moderate binding ability with CASP3 and CASP8. Conclusion. In this study, the material basis and potential pharmacological mechanisms of KP-induced liver injury were preliminarily explored. Our research provides the initial theoretical basis for reducing the toxicity of KP.</description><subject>Animal research</subject><subject>Apoptosis</subject><subject>Chinese medicine</subject><subject>Drug dosages</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Hepatotoxicity</subject><subject>Inflammation</subject><subject>Interleukin 17</subject><subject>Laboratory animals</subject><subject>Liver</subject><subject>Metabolism</subject><subject>Methoxsalen</subject><subject>Pharmacology</subject><subject>Psoriasis</subject><subject>Software</subject><subject>Toxicity</subject><subject>Tumor necrosis factor-α</subject><issn>1741-427X</issn><issn>1741-4288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kcFv0zAUhyMEYmNw44wscZkEYbYTx8kFaVRjqyiwA0jcrFf7ZXFJ7GInGz3wv-OqpRocONny-_zp_fTLsueMvmFMiDNOOT9rGlY1ZfMgO2ayZHnJ6_rh4S6_HWVPYlxRyhsp5ePsqKgEq2vBj7NfFz_XvQ8wWu-Ib8nYIZn5Ye0dujEScIZcdxAG0L73N1ZDTz6i7sDZOMTthw-4sY5c277P585MGg1Z2FsMZO5WU9iQdxDTU5J_wvHOh-_3dZun2aMW-ojP9udJ9vX9xZfZVb74fDmfnS9yXVIx5mlb0-CS8bLlDGnNKyy5BloZFEVteE2xXUrNtSigAiMQoC0AwIBm0NZNcZK93XnX03JAo1O2AL1aBztA2CgPVv09cbZTN_5WNbIsKyaT4HQvCP7HhHFUg40a-x4c-ikqLkVZi6qQIqEv_0FXfgouxdtSohC0ojRRr3eUDj7GgO1hGUbVtle17VXte034i_sBDvCfIhPwagd01hm4s__X_Qa__K20</recordid><startdate>2022</startdate><enddate>2022</enddate><creator>Xing, Bo</creator><creator>Cui, Yaling</creator><creator>Chen, Ying</creator><creator>Lai, Lingyun</creator><creator>Zhang, Meiling</creator><creator>Xu, Xiangbo</creator><creator>Wang, Nan</creator><creator>Jiang, Xiaowen</creator><creator>Xu, Zihua</creator><creator>Zhao, Qingchun</creator><general>Hindawi</general><general>Hindawi Limited</general><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7T5</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88G</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M2M</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-9168-7316</orcidid><orcidid>https://orcid.org/0000-0003-2011-274X</orcidid><orcidid>https://orcid.org/0000-0001-9963-9100</orcidid><orcidid>https://orcid.org/0000-0002-8561-6810</orcidid><orcidid>https://orcid.org/0000-0003-0381-9794</orcidid><orcidid>https://orcid.org/0000-0002-0840-3096</orcidid><orcidid>https://orcid.org/0000-0001-6295-4887</orcidid><orcidid>https://orcid.org/0000-0001-9256-9971</orcidid><orcidid>https://orcid.org/0000-0001-8246-7058</orcidid><orcidid>https://orcid.org/0000-0003-2386-2570</orcidid></search><sort><creationdate>2022</creationdate><title>Exploration of the Components and Pharmacological Mechanisms of Keyin Pill-Induced Liver Injury Based on Network Pharmacology</title><author>Xing, Bo ; 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Keyin pill (KP), a patented medicine in China, is used to treat psoriasis. However, KP has been reported to have liver toxicity, but its toxic substance basis and underlying mechanisms remain unclear. Therefore, this study aimed to explore the pharmacological mechanisms and components of KP-induced liver injury through animal experiments, UPLC-QTOF/MS combined with network pharmacology. Methods. Firstly, based on the immune stress mouse model, liver function parameters and hematoxylin-eosin (H&E) staining were detected to investigate KP-induced liver injury. The UPLC-QTOF/MS method was used to identify the components of KP. CTD database and literature mining were further applied to screen nonliver protective components. Subsequently, the nonliver protective components and their corresponding targets and targets of hepatotoxicity were analyzed by the method of network pharmacology. Finally, key targets from networked pharmacology were examined by the enzyme-linked immunosorbent assay (ELISA) and molecular docking. Results. Our results indicated that KP had hepatotoxicity in male Kunming mice, which could favor hepatocyte necrosis and infiltration of inflammatory cells. A total of 70 nonliver protective compounds were identified and screened. The results of network pharmacology illustrated that methoxsalen, obacunone, limonin, and dictamnine might be the main compounds that caused liver damage. The potential hepatotoxicity mechanisms of KP might be through the IL17 and apoptosis pathways to regulate IL6, TNFα, CASP3, and CASP8 targets, thereby causing inflammation, excessive release of factors, and hepatocyte necrosis. The results of the ELISA experiments indicated that KP could increase the release of IL6 and TNFα inflammatory factors in liver tissues. Molecular docking suggested that methoxsalen, obacunone, limonin, and dictamnine had moderate binding ability with CASP3 and CASP8. Conclusion. In this study, the material basis and potential pharmacological mechanisms of KP-induced liver injury were preliminarily explored. Our research provides the initial theoretical basis for reducing the toxicity of KP.</abstract><cop>United States</cop><pub>Hindawi</pub><pmid>36518852</pmid><doi>10.1155/2022/9916949</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-9168-7316</orcidid><orcidid>https://orcid.org/0000-0003-2011-274X</orcidid><orcidid>https://orcid.org/0000-0001-9963-9100</orcidid><orcidid>https://orcid.org/0000-0002-8561-6810</orcidid><orcidid>https://orcid.org/0000-0003-0381-9794</orcidid><orcidid>https://orcid.org/0000-0002-0840-3096</orcidid><orcidid>https://orcid.org/0000-0001-6295-4887</orcidid><orcidid>https://orcid.org/0000-0001-9256-9971</orcidid><orcidid>https://orcid.org/0000-0001-8246-7058</orcidid><orcidid>https://orcid.org/0000-0003-2386-2570</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Animal research Apoptosis Chinese medicine Drug dosages Enzyme-linked immunosorbent assay Hepatotoxicity Inflammation Interleukin 17 Laboratory animals Liver Metabolism Methoxsalen Pharmacology Psoriasis Software Toxicity Tumor necrosis factor-α |
title | Exploration of the Components and Pharmacological Mechanisms of Keyin Pill-Induced Liver Injury Based on Network Pharmacology |
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