Fangchinoline protects hepatic ischemia/reperfusion liver injury in rats through anti‐oxidative stress and anti‐inflammation properties: an in silico study
Liver ischemia‐reperfusion (I/R) injury is a common cause of organ failure, developed by a sudden block in the blood and oxygen supply and subsequent restoration. I/R damage is responsible for acute and chronic rejection after organ transplantation, accounting for 10% of early graft failure. The stu...
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Veröffentlicht in: | Biotechnology and applied biochemistry 2024-12, Vol.71 (6), p.1281-1292 |
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description | Liver ischemia‐reperfusion (I/R) injury is a common cause of organ failure, developed by a sudden block in the blood and oxygen supply and subsequent restoration. I/R damage is responsible for acute and chronic rejection after organ transplantation, accounting for 10% of early graft failure. The study investigated the therapeutic properties of fangchinoline in liver injury‐induced rats. The rats were divided into three groups: Sham, I/R without pretreatment, and I/R + 10 mg/kg fangchinoline pretreatment. Blood and liver samples were collected for assays, and an in silico docking analysis was conducted to determine fangchinoline's inhibitory effect. The pretreatment with 10 mg/kg of fangchinoline effectively reduced hepatic marker enzymes such as AST, LDH, and ALT in the serum of rats with liver I/R damage. Fangchinoline treatment significantly reduced interleukin‐8 (IL‐8), IL‐6, and tumor necrosis factor‐α (TNF‐α) in I/R‐induced rats, boosting antioxidants and decreasing MDA. Histopathological studies showed liver injury protection, and fangchinoline inhibited TNF‐α and IL‐6 with improved binding affinity. Fangchinoline has hepatoprotective properties by reducing inflammation in rats with liver I/R damage, as demonstrated in the current study. Hence, it can be an effective salutary agent in preventing liver damage caused by I/R. |
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I/R damage is responsible for acute and chronic rejection after organ transplantation, accounting for 10% of early graft failure. The study investigated the therapeutic properties of fangchinoline in liver injury‐induced rats. The rats were divided into three groups: Sham, I/R without pretreatment, and I/R + 10 mg/kg fangchinoline pretreatment. Blood and liver samples were collected for assays, and an in silico docking analysis was conducted to determine fangchinoline's inhibitory effect. The pretreatment with 10 mg/kg of fangchinoline effectively reduced hepatic marker enzymes such as AST, LDH, and ALT in the serum of rats with liver I/R damage. Fangchinoline treatment significantly reduced interleukin‐8 (IL‐8), IL‐6, and tumor necrosis factor‐α (TNF‐α) in I/R‐induced rats, boosting antioxidants and decreasing MDA. Histopathological studies showed liver injury protection, and fangchinoline inhibited TNF‐α and IL‐6 with improved binding affinity. Fangchinoline has hepatoprotective properties by reducing inflammation in rats with liver I/R damage, as demonstrated in the current study. Hence, it can be an effective salutary agent in preventing liver damage caused by I/R.</description><identifier>ISSN: 0885-4513</identifier><identifier>ISSN: 1470-8744</identifier><identifier>EISSN: 1470-8744</identifier><identifier>DOI: 10.1002/bab.2628</identifier><identifier>PMID: 38984607</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Animals ; Anti-Inflammatory Agents - chemistry ; Anti-Inflammatory Agents - pharmacology ; Antioxidants - chemistry ; Antioxidants - metabolism ; Antioxidants - pharmacology ; Benzylisoquinolines - chemistry ; Benzylisoquinolines - pharmacology ; Blood ; Computer Simulation ; Damage prevention ; Enzyme inhibitors ; fangchinoline ; Graft rejection ; hepatoprotection ; Inflammation ; Injury prevention ; Interleukin 6 ; Ischemia ; ischemia/reperfusion ; Liver ; Liver - drug effects ; Liver - metabolism ; Liver - pathology ; liver injury ; Liver transplantation ; Male ; Molecular Docking Simulation ; Oxidative stress ; Oxidative Stress - drug effects ; Pretreatment ; Rats ; Rats, Wistar ; Reperfusion ; Reperfusion Injury - drug therapy ; Reperfusion Injury - metabolism ; Reperfusion Injury - pathology ; Reperfusion Injury - prevention & control ; Tumor necrosis factor ; Tumor necrosis factor-TNF ; Xenografts</subject><ispartof>Biotechnology and applied biochemistry, 2024-12, Vol.71 (6), p.1281-1292</ispartof><rights>2024 International Union of Biochemistry and Molecular Biology, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c3108-17ae7b8702ed62f19d21d9202d289883cd86a8da054213e37e509f4b9be520653</cites><orcidid>0009-0006-2937-6644</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fbab.2628$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fbab.2628$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38984607$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Shuangxi</creatorcontrib><creatorcontrib>Xiang, AnDong</creatorcontrib><creatorcontrib>Guo, Feng</creatorcontrib><creatorcontrib>Alarfaj, Abdullah A.</creatorcontrib><creatorcontrib>Gao, Zehai</creatorcontrib><title>Fangchinoline protects hepatic ischemia/reperfusion liver injury in rats through anti‐oxidative stress and anti‐inflammation properties: an in silico study</title><title>Biotechnology and applied biochemistry</title><addtitle>Biotechnol Appl Biochem</addtitle><description>Liver ischemia‐reperfusion (I/R) injury is a common cause of organ failure, developed by a sudden block in the blood and oxygen supply and subsequent restoration. I/R damage is responsible for acute and chronic rejection after organ transplantation, accounting for 10% of early graft failure. The study investigated the therapeutic properties of fangchinoline in liver injury‐induced rats. The rats were divided into three groups: Sham, I/R without pretreatment, and I/R + 10 mg/kg fangchinoline pretreatment. Blood and liver samples were collected for assays, and an in silico docking analysis was conducted to determine fangchinoline's inhibitory effect. The pretreatment with 10 mg/kg of fangchinoline effectively reduced hepatic marker enzymes such as AST, LDH, and ALT in the serum of rats with liver I/R damage. Fangchinoline treatment significantly reduced interleukin‐8 (IL‐8), IL‐6, and tumor necrosis factor‐α (TNF‐α) in I/R‐induced rats, boosting antioxidants and decreasing MDA. Histopathological studies showed liver injury protection, and fangchinoline inhibited TNF‐α and IL‐6 with improved binding affinity. Fangchinoline has hepatoprotective properties by reducing inflammation in rats with liver I/R damage, as demonstrated in the current study. Hence, it can be an effective salutary agent in preventing liver damage caused by I/R.</description><subject>Animals</subject><subject>Anti-Inflammatory Agents - chemistry</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Antioxidants - chemistry</subject><subject>Antioxidants - metabolism</subject><subject>Antioxidants - pharmacology</subject><subject>Benzylisoquinolines - chemistry</subject><subject>Benzylisoquinolines - pharmacology</subject><subject>Blood</subject><subject>Computer Simulation</subject><subject>Damage prevention</subject><subject>Enzyme inhibitors</subject><subject>fangchinoline</subject><subject>Graft rejection</subject><subject>hepatoprotection</subject><subject>Inflammation</subject><subject>Injury prevention</subject><subject>Interleukin 6</subject><subject>Ischemia</subject><subject>ischemia/reperfusion</subject><subject>Liver</subject><subject>Liver - drug effects</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>liver injury</subject><subject>Liver transplantation</subject><subject>Male</subject><subject>Molecular Docking Simulation</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Pretreatment</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reperfusion</subject><subject>Reperfusion Injury - drug therapy</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - pathology</subject><subject>Reperfusion Injury - prevention & control</subject><subject>Tumor necrosis factor</subject><subject>Tumor necrosis factor-TNF</subject><subject>Xenografts</subject><issn>0885-4513</issn><issn>1470-8744</issn><issn>1470-8744</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kU9u1TAQhy0Eoo-CxAlQJDZs0vpfYptdW1FAqsQG1pYTTxo_JfbDTgpvxxG4AXfjJMyjLUhIrEbyfPN5Rj9CnjN6wijlp53rTnjL9QOyYVLRWispH5IN1bqpZcPEEXlSypZSqpXmj8mR0EbLlqoN-XHp4nU_hpimEKHa5bRAv5RqhJ1bQl-F0o8wB3eaYQd5WEtIsZrCDeQqxO2a91iq7HBiGXNar8fKxSX8_PY9fQ0eDTdQlSVDKfju73shDpObZ2yjDL9E8xKgvMb-QVfCFPqEc6vfPyWPBjcVeHZXj8mnyzcfL97VVx_evr84u6p7waiumXKgOq0oB9_ygRnPmTeccs_xVC16r1unvaON5EyAUNBQM8jOdNBw2jbimLy69eI6n1coi53xdJgmFyGtxQqqlDHS0BbRl_-g27TmiNtZwSQzLSbA_wr7nErJMNhdDrPLe8uoPYRmMTR7CA3RF3fCtZvB_wHvU0KgvgW-hAn2_xXZ87Pz38Jf3hGlBg</recordid><startdate>202412</startdate><enddate>202412</enddate><creator>Li, Shuangxi</creator><creator>Xiang, AnDong</creator><creator>Guo, Feng</creator><creator>Alarfaj, Abdullah A.</creator><creator>Gao, Zehai</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7TB</scope><scope>7TK</scope><scope>7U5</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>L7M</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0009-0006-2937-6644</orcidid></search><sort><creationdate>202412</creationdate><title>Fangchinoline protects hepatic ischemia/reperfusion liver injury in rats through anti‐oxidative stress and anti‐inflammation properties: an in silico study</title><author>Li, Shuangxi ; 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I/R damage is responsible for acute and chronic rejection after organ transplantation, accounting for 10% of early graft failure. The study investigated the therapeutic properties of fangchinoline in liver injury‐induced rats. The rats were divided into three groups: Sham, I/R without pretreatment, and I/R + 10 mg/kg fangchinoline pretreatment. Blood and liver samples were collected for assays, and an in silico docking analysis was conducted to determine fangchinoline's inhibitory effect. The pretreatment with 10 mg/kg of fangchinoline effectively reduced hepatic marker enzymes such as AST, LDH, and ALT in the serum of rats with liver I/R damage. Fangchinoline treatment significantly reduced interleukin‐8 (IL‐8), IL‐6, and tumor necrosis factor‐α (TNF‐α) in I/R‐induced rats, boosting antioxidants and decreasing MDA. Histopathological studies showed liver injury protection, and fangchinoline inhibited TNF‐α and IL‐6 with improved binding affinity. Fangchinoline has hepatoprotective properties by reducing inflammation in rats with liver I/R damage, as demonstrated in the current study. Hence, it can be an effective salutary agent in preventing liver damage caused by I/R.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>38984607</pmid><doi>10.1002/bab.2628</doi><tpages>12</tpages><orcidid>https://orcid.org/0009-0006-2937-6644</orcidid></addata></record> |
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subjects | Animals Anti-Inflammatory Agents - chemistry Anti-Inflammatory Agents - pharmacology Antioxidants - chemistry Antioxidants - metabolism Antioxidants - pharmacology Benzylisoquinolines - chemistry Benzylisoquinolines - pharmacology Blood Computer Simulation Damage prevention Enzyme inhibitors fangchinoline Graft rejection hepatoprotection Inflammation Injury prevention Interleukin 6 Ischemia ischemia/reperfusion Liver Liver - drug effects Liver - metabolism Liver - pathology liver injury Liver transplantation Male Molecular Docking Simulation Oxidative stress Oxidative Stress - drug effects Pretreatment Rats Rats, Wistar Reperfusion Reperfusion Injury - drug therapy Reperfusion Injury - metabolism Reperfusion Injury - pathology Reperfusion Injury - prevention & control Tumor necrosis factor Tumor necrosis factor-TNF Xenografts |
title | Fangchinoline protects hepatic ischemia/reperfusion liver injury in rats through anti‐oxidative stress and anti‐inflammation properties: an in silico study |
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