乙酰-11-酮- β乳香酸对苯并(a)芘中毒条件下肝膜动力学和脂质组的影响

Rishav Puri , Priti Bhardwaj , Sunil Kumar Dhatwalia, Devinder Kumar Dhawan
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引用次数: 0

摘要

背景和目的污染和生活方式的改变使人类暴露于多种有毒物质,如可能导致危及生命的疾病的多环芳烃。本研究旨在阐明乙酰-11-酮- β乳香酸(AKBA)在含苯并(a)芘(BaP)诱导的雌性大鼠肝膜动力学和脂质组改变中的保护作用。实验方法将动物分为5组,即正常对照组、载药组、BaP组、AKBA组和BaP + AKBA组。为了诱导肝毒性,BaP以50 mg/kg b.wt的剂量口服。每周用橄榄油溶解两次,持续4周。在BaP治疗前4周补充AKBA,并以50 mg/kg b.wt的剂量水平持续8周。一周三次。研究了氧化应激生物标志物、膜脂质谱、膜流动性参数和atp酶活性等关键指标。结果与结论苯并(a)芘处理导致大鼠脂质过氧化(LPO)和ROS水平显著升高,而总脂质、磷脂、胆固醇、糖脂质水平和atp酶活性显著降低。用1,6-二苯基-1,3,5-己三烯(DPH)和芘荧光探针测定,BaP中毒大鼠肝膜流动性显著增加。有趣的是,在BaP处理的大鼠中添加AKBA明显改变了膜动力学和脂质组,并通过破坏氧化应激标记物的活性来调节肝毒性,并改善了肝脏组织结构。因此,我们的研究得出结论,AKBA可以作为一种预防性干预,为肝细胞提供保护,因为它在BaP诱导的毒性条件下保持膜的完整性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Influence of acetyl-11-keto-beta boswellic acid on hepatic membrane dynamics and lipidiome during conditions of benzo(a)pyrene induced toxicity

Background and Aim

Pollution and lifestyle changes expose mankind to a number of toxicants such as polycyclic aromatic hydrocarbons that may cause life-threatening diseases. The present study was undertaken to explicate the protective role of Acetyl-11-Keto-Beta Boswellic Acid (AKBA), if any, in containing benzo(a)pyrene (BaP) induced alterations on hepatic membrane dynamics and lipidiome in female rats.

Experimental procedure

The animals were divided into five groups viz. Normal control, Vehicle treated, BaP treated, AKBA treated and BaP + AKBA treated. To induce hepatotoxicity, BaP was administered orally at a dose level of 50 mg/kg b.wt. dissolved in olive oil twice a week for 4 weeks. AKBA was supplemented to animals four weeks prior to BaP treatment and continued for 8 weeks at a dose level of 50 mg/kg b.wt. thrice a week. Certain key indices that included oxidative stress biomarkers, lipid profile of membranes, membrane fluidity parameters and activities of ATPases were studied.

Results and Conclusion

The results showed that benzo(a)pyrene treatment resulted in a significant increase in the levels of lipid peroxidation (LPO) and ROS but caused a significant decrease in the levels of total lipids, phospholipids, cholesterol, glycolipids and activities of ATPases. Hepatic membrane fluidity as assessed by 1,6-Diphenyl-1,3,5-hexatriene (DPH) and Pyrene fluorescence probes was significantly increased in rats intoxicated with BaP. Interestingly, AKBA supplementation to BaP treated rats appreciably contained altered membrane dynamics and lipidiome as well as modulated hepatotoxicity by skirmishing activities of oxidative stress markers and also improved hepatic histoarchitecture. Our study thus concludes that AKBA can be used as a prophylactic intervention in providing protection to hepatocytes as it maintains membrane integrity in conditions of BaP induced toxicity.

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