Ghadeer M Albadrani, Ahmed E Altyar, Osama A Kensara, Mohie A M Haridy, Mohamed Sayed Zaazouee, Alaa Ahmed Elshanbary, Amany A Sayed, Mohamed M Abdel-Daim
{"title":"肉毒碱对黄曲霉毒素 B1 诱导的大鼠肝、肾和心脏毒性的抗氧化、抗炎和抗 DNA 损伤作用。","authors":"Ghadeer M Albadrani, Ahmed E Altyar, Osama A Kensara, Mohie A M Haridy, Mohamed Sayed Zaazouee, Alaa Ahmed Elshanbary, Amany A Sayed, Mohamed M Abdel-Daim","doi":"10.1093/toxres/tfae083","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Aflatoxin B1 (AFB1) food contamination is a global health hazard that has detrimental effects on both human and animal health. The objective of the current study is to assess the protective impact of carnosic acid against AFB1-induced toxicities in the liver, kidneys, and heart.</p><p><strong>Methods: </strong>Forty male Wistar Albino rats (weighting 180 ~ 200 g) were allocated into 5 groups (8 rats each); the 1<sup>st</sup> group received saline as served as a control, the 2<sup>nd</sup> group received carnosic acid (CA100) at a dose of 100 mg/kg bw/day by gavage for 14 days, the 3<sup>rd</sup> group received AFB1 at a dose of 2.5 mg/kg bw, orally twice on days 12 and 14, the 4<sup>th</sup> group (AFB1-CA50) received AFB1 as in the 3<sup>rd</sup> group and CA at a dose of 50 mg/kg bw/day, and the 5<sup>th</sup> group (AFB1-CA100) received AFB1 as in the 3<sup>rd</sup> group and CA as in the 2<sup>nd</sup> group.</p><p><strong>Results: </strong>CA significantly decreased the liver enzymes (ALT, AST. ALP), renal function products (LDH, BUN, creatinine), and cardiac enzymes (CK and CK-MB) to control levels after the high increment by AFB1 exposure. Moreover, CA significantly decreased the oxidative stress (MDA, NO, 8-OHdG) and increased the antioxidant enzyme activities (CAT, GSH, GSH-Px, and SOD) after severe disruption of oxidant/antioxidant balance by AFB1 exposure. Interestingly, CA significantly decreased the proinflammatory mediators (IL-6, IL-1β, and TNF-α) to the control levels after severe inflammation induced by AFB1 exposure.</p><p><strong>Conclusions: </strong>Conclusively, CA had antioxidant, anti-inflammatory, and anti-DNA damage effects against hepatic, renal, and cardiac AFB1-induced toxicities.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":null,"pages":null},"PeriodicalIF":2.2000,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11200098/pdf/","citationCount":"0","resultStr":"{\"title\":\"Antioxidant, anti-inflammatory, and anti-DNA damage effects of carnosic acid against aflatoxin B1-induced hepatic, renal, and cardiac toxicities in rats.\",\"authors\":\"Ghadeer M Albadrani, Ahmed E Altyar, Osama A Kensara, Mohie A M Haridy, Mohamed Sayed Zaazouee, Alaa Ahmed Elshanbary, Amany A Sayed, Mohamed M Abdel-Daim\",\"doi\":\"10.1093/toxres/tfae083\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Aflatoxin B1 (AFB1) food contamination is a global health hazard that has detrimental effects on both human and animal health. The objective of the current study is to assess the protective impact of carnosic acid against AFB1-induced toxicities in the liver, kidneys, and heart.</p><p><strong>Methods: </strong>Forty male Wistar Albino rats (weighting 180 ~ 200 g) were allocated into 5 groups (8 rats each); the 1<sup>st</sup> group received saline as served as a control, the 2<sup>nd</sup> group received carnosic acid (CA100) at a dose of 100 mg/kg bw/day by gavage for 14 days, the 3<sup>rd</sup> group received AFB1 at a dose of 2.5 mg/kg bw, orally twice on days 12 and 14, the 4<sup>th</sup> group (AFB1-CA50) received AFB1 as in the 3<sup>rd</sup> group and CA at a dose of 50 mg/kg bw/day, and the 5<sup>th</sup> group (AFB1-CA100) received AFB1 as in the 3<sup>rd</sup> group and CA as in the 2<sup>nd</sup> group.</p><p><strong>Results: </strong>CA significantly decreased the liver enzymes (ALT, AST. ALP), renal function products (LDH, BUN, creatinine), and cardiac enzymes (CK and CK-MB) to control levels after the high increment by AFB1 exposure. Moreover, CA significantly decreased the oxidative stress (MDA, NO, 8-OHdG) and increased the antioxidant enzyme activities (CAT, GSH, GSH-Px, and SOD) after severe disruption of oxidant/antioxidant balance by AFB1 exposure. Interestingly, CA significantly decreased the proinflammatory mediators (IL-6, IL-1β, and TNF-α) to the control levels after severe inflammation induced by AFB1 exposure.</p><p><strong>Conclusions: </strong>Conclusively, CA had antioxidant, anti-inflammatory, and anti-DNA damage effects against hepatic, renal, and cardiac AFB1-induced toxicities.</p>\",\"PeriodicalId\":105,\"journal\":{\"name\":\"Toxicology Research\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.2000,\"publicationDate\":\"2024-05-31\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11200098/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Toxicology Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1093/toxres/tfae083\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/6/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q3\",\"JCRName\":\"TOXICOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Toxicology Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1093/toxres/tfae083","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/6/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"TOXICOLOGY","Score":null,"Total":0}
Antioxidant, anti-inflammatory, and anti-DNA damage effects of carnosic acid against aflatoxin B1-induced hepatic, renal, and cardiac toxicities in rats.
Background: Aflatoxin B1 (AFB1) food contamination is a global health hazard that has detrimental effects on both human and animal health. The objective of the current study is to assess the protective impact of carnosic acid against AFB1-induced toxicities in the liver, kidneys, and heart.
Methods: Forty male Wistar Albino rats (weighting 180 ~ 200 g) were allocated into 5 groups (8 rats each); the 1st group received saline as served as a control, the 2nd group received carnosic acid (CA100) at a dose of 100 mg/kg bw/day by gavage for 14 days, the 3rd group received AFB1 at a dose of 2.5 mg/kg bw, orally twice on days 12 and 14, the 4th group (AFB1-CA50) received AFB1 as in the 3rd group and CA at a dose of 50 mg/kg bw/day, and the 5th group (AFB1-CA100) received AFB1 as in the 3rd group and CA as in the 2nd group.
Results: CA significantly decreased the liver enzymes (ALT, AST. ALP), renal function products (LDH, BUN, creatinine), and cardiac enzymes (CK and CK-MB) to control levels after the high increment by AFB1 exposure. Moreover, CA significantly decreased the oxidative stress (MDA, NO, 8-OHdG) and increased the antioxidant enzyme activities (CAT, GSH, GSH-Px, and SOD) after severe disruption of oxidant/antioxidant balance by AFB1 exposure. Interestingly, CA significantly decreased the proinflammatory mediators (IL-6, IL-1β, and TNF-α) to the control levels after severe inflammation induced by AFB1 exposure.
Conclusions: Conclusively, CA had antioxidant, anti-inflammatory, and anti-DNA damage effects against hepatic, renal, and cardiac AFB1-induced toxicities.