Albadrani Ghadeer M, Altyar Ahmed E, Kensara Osama A, Haridy Mohie A M, Zaazouee Mohamed Sayed, Elshanbary Alaa Ahmed, Sayed Amany A, Abdel-Daim Mohamed M
Department of Biology, College of Science, Princess Nourah bint Abdulrahman University, PO Box 84428, Riyadh 11671, Saudi Arabia.
Department of Pharmacy Practice, Faculty of Pharmacy, King Abdulaziz University, P.O. Box 80260, Jeddah 21589, Saudi Arabia.
Toxicol Res (Camb). 2024 May 31;13(3):tfae083. doi: 10.1093/toxres/tfae083. eCollection 2024 Jun.
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.
Forty male Wistar Albino rats (weighting 180 ~ 200 g) were allocated into 5 groups (8 rats each); the 1 group received saline as served as a control, the 2 group received carnosic acid (CA100) at a dose of 100 mg/kg bw/day by gavage for 14 days, the 3 group received AFB1 at a dose of 2.5 mg/kg bw, orally twice on days 12 and 14, the 4 group (AFB1-CA50) received AFB1 as in the 3 group and CA at a dose of 50 mg/kg bw/day, and the 5 group (AFB1-CA100) received AFB1 as in the 3 group and CA as in the 2 group.
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.
Conclusively, CA had antioxidant, anti-inflammatory, and anti-DNA damage effects against hepatic, renal, and cardiac AFB1-induced toxicities.
黄曲霉毒素B1（AFB1）污染食品是一种全球性的健康危害，对人类和动物健康均有不利影响。本研究的目的是评估肌醇六磷酸对AFB1诱导的肝脏、肾脏和心脏毒性的保护作用。
将40只雄性Wistar白化大鼠（体重180~200 g）分为5组（每组8只）；第1组给予生理盐水作为对照，第2组通过灌胃给予剂量为100 mg/kg体重/天的肌醇六磷酸，持续14天，第3组在第12天和第14天口服给予剂量为2.5 mg/kg体重的AFB1，第4组（AFB1-CA50）给予与第3组相同剂量的AFB1和剂量为50 mg/kg体重/天的肌醇六磷酸，第5组（AFB1-CA100）给予与第3组相同剂量的AFB1和与第2组相同剂量的肌醇六磷酸。
AFB1暴露导致各项指标大幅升高后，肌醇六磷酸显著降低了肝酶（ALT、AST、ALP）、肾功能指标（LDH、BUN、肌酐）和心肌酶（CK和CK-MB）水平至对照水平。此外，AFB1暴露严重破坏氧化还原平衡后，肌醇六磷酸显著降低了氧化应激（MDA、NO、8-羟基脱氧鸟苷）并提高了抗氧化酶活性（CAT、GSH、GSH-Px和SOD）。有趣的是，AFB1暴露引发严重炎症后，肌醇六磷酸显著降低了促炎介质（IL-6、IL-1β和TNF-α）水平至对照水平。
总之，肌醇六磷酸对AFB1诱导的肝脏、肾脏和心脏毒性具有抗氧化、抗炎和抗DNA损伤作用。
