Department of Medical Pharmacology, Faculty of Medicine, Gazi University, Ankara, Turkey.
Ankara Medipol University, Faculty of Pharmacy, Ankara, Turkey.
Toxicon. 2024 Aug 28;247:107854. doi: 10.1016/j.toxicon.2024.107854. Epub 2024 Jul 6.
The consumption of mushrooms containing α-Amanitin (α-A) can lead to severe liver damage. In this study, toxicological experiments were conducted to confirm the protective effects of pomegranate seed oil (PSO) and black cumin oil (BCO) against α-A-induced hepatotoxicity. Rats exposed once to α-A (3 mg/kg bw, i.p.) or saline alone (0.1 ml, i.p.) were either left untreated or treated with PSO or BCO at a dose of 2 ml/kg bw/day by oral gavage on the same day, and the treatment was continued for 7 days. Serum aminotransferases (ALT and AST), alkaline phosphatase (ALP) and total protein levels were measured and the active caspase 3 (cl-caspase 3) was evaluated by western blotting in the liver. Serum ALT, AST and ALP levels tended to decrease in the α-A exposed group, but no statistically significant difference was found compared to the saline group (p > 0.05). PSO and BCO did not affect serum liver function tests in rats exposed to saline or α-A. α-A toxicity was demonstrated by a significant decrease in serum total protein level (p < 0.05), a significant increase in liver cl-caspase 3 expression (p < 0.05), and structural liver damage mainly characterized by mononuclear inflammation and steatosis. When α-A exposed rats were treated with BCO, the increase in cl-caspase 3 was not inhibited, on the contrary BCO increased cl-caspase 3 in healthy rats (p < 0.05). PSO significantly ameliorated α-A-induced cl-caspase 3 increase and inflammatory histopathology in the liver. Both PSO and BCO completely prevented α-A-induced protein degradation. The findings indicate that PSO and BCO may protect liver functions against α-A-induced hepatotoxicity, encouraging future comprehensive studies to test them at different doses and frequency.
食用含有α-鹅膏蕈碱（α-A）的蘑菇会导致严重的肝损伤。在这项研究中，进行了毒理学实验以确认石榴籽油（PSO）和黑孜然油（BCO）对α-A 诱导的肝毒性的保护作用。大鼠单次暴露于α-A（3mg/kg bw，ip）或单独生理盐水（0.1ml，ip），未处理或用 PSO 或 BCO 以 2ml/kg bw/天的剂量经口灌胃，同一天开始治疗，持续 7 天。测定血清氨基转移酶（ALT 和 AST）、碱性磷酸酶（ALP）和总蛋白水平，并通过western blot 测定肝中活性半胱天冬酶 3（cl-caspase 3）。α-A 暴露组血清 ALT、AST 和 ALP 水平趋于降低，但与生理盐水组相比无统计学差异（p>0.05）。PSO 和 BCO 对暴露于生理盐水或α-A 的大鼠的血清肝功能试验没有影响。α-A 毒性表现为血清总蛋白水平显著降低（p<0.05）、肝 cl-caspase 3 表达显著增加（p<0.05）以及以单核炎症和脂肪变性为特征的结构肝损伤。当α-A 暴露大鼠用 BCO 治疗时，cl-caspase 3 的增加未被抑制，相反 BCO 增加了健康大鼠的 cl-caspase 3（p<0.05）。PSO 显著改善了α-A 诱导的 cl-caspase 3 增加和肝组织病理学炎症。PSO 和 BCO 完全阻止了α-A 诱导的蛋白降解。研究结果表明，PSO 和 BCO 可能保护肝脏功能免受α-A 诱导的肝毒性，鼓励未来进行不同剂量和频率的综合研究来测试它们。
