PDF(Pubmed)
Abstract：
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: Conclusively, CA had antioxidant, anti-inflammatory, and anti-DNA damage effects against hepatic, renal, and cardiac AFB1-induced toxicities.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: Conclusively, CA had antioxidant, anti-inflammatory, and anti-DNA damage effects against hepatic, renal, and cardiac AFB1-induced toxicities.
摘要：
■黄曲霉毒素B1（AFB1）食品污染是一种全球性的健康危害，对人类和动物的健康都有不利影响。本研究的目的是评估鼠尾草酸对AFB1诱导的肝脏毒性的保护作用，肾脏，和心脏。
■将40只雄性Wistar白化病大鼠（体重180〜200g）分为5组（每组8只）；第一组接受生理盐水作为对照组，第2组接受剂量为100mg/kgbw/天的鼠尾草酸（CA100），为期14天，第三组以2.5mg/kgbw的剂量接受AFB1，在第12天和第14天口服两次，第4组（AFB1-CA50）与第3组一样接受AFB1，并以50mg/kgbw/天的剂量接受CA，第5组（AFB1-CA100）与第3组一样接受AFB1，与第2组一样接受CA。
■CA显着降低肝酶（ALT，AST.ALP),肾功能产品（LDH，BUN,肌酐)，AFB1暴露后，心肌酶（CK和CK-MB）升高至对照水平。此外，CA显著降低氧化应激(MDA,NO,8-OHdG)和增加抗氧化酶活性(CAT，GSH,GSH-Px,和SOD）在AFB1暴露严重破坏氧化剂/抗氧化剂平衡后。有趣的是,CA显着降低促炎介质（IL-6，IL-1β，和TNF-α）在AFB1暴露引起的严重炎症后达到对照水平。
■最后，CA有抗氧化剂，抗炎,和抗DNA损伤作用对肝脏，肾,和心脏AFB1诱导的毒性。
■将40只雄性Wistar白化病大鼠（体重180〜200g）分为5组（每组8只）；第一组接受生理盐水作为对照组，第2组接受剂量为100mg/kgbw/天的鼠尾草酸（CA100），为期14天，第三组以2.5mg/kgbw的剂量接受AFB1，在第12天和第14天口服两次，第4组（AFB1-CA50）与第3组一样接受AFB1，并以50mg/kgbw/天的剂量接受CA，第5组（AFB1-CA100）与第3组一样接受AFB1，与第2组一样接受CA。
■CA显着降低肝酶（ALT，AST.ALP),肾功能产品（LDH，BUN,肌酐)，AFB1暴露后，心肌酶（CK和CK-MB）升高至对照水平。此外，CA显著降低氧化应激(MDA,NO,8-OHdG)和增加抗氧化酶活性(CAT，GSH,GSH-Px,和SOD）在AFB1暴露严重破坏氧化剂/抗氧化剂平衡后。有趣的是,CA显着降低促炎介质（IL-6，IL-1β，和TNF-α）在AFB1暴露引起的严重炎症后达到对照水平。
■最后，CA有抗氧化剂，抗炎,和抗DNA损伤作用对肝脏，肾,和心脏AFB1诱导的毒性。
