姜黄作为一种治疗剂,可防止砷诱导的大鼠模型代谢失调

Adewale Adetutu , Abiodun Bukunmi Aborisade , Temitope Deborah Olaniyi
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引用次数: 0

摘要

民族药理学相关性砷等金属类物质的摄入对健康造成的危害已成为全球关注的问题。本研究旨在评估姜黄对砷引起的大鼠血脂和能量代谢改变的保护作用:第 1 组(对照组)接受标准大鼠饲料;第 2 组接受砷饮食;第 3 组接受砷加姜黄补充饮食。收集血液和肝脏组织样本,利用 qRT-PCR 技术检测血脂概况、血糖水平、能量代谢参数和 PPAR-α mRNA 表达。结果表明,180 天后,砷暴露大鼠的血脂含量显著增加(p<0.05),增加了冠状动脉疾病的风险。砷暴露组和姜黄暴露组在 90 天和 180 天后的总胆固醇(TC)、甘油三酯(TG)和低密度脂蛋白(LDL)水平都有所升高,细微的差异表明存在血脂异常和动脉粥样硬化。血糖观察显示,砷暴露大鼠最初出现低血糖,180 天后发展为高血糖。180 天后,砷明显(p<0.05)抑制了肝脏中丙酮酸激酶、己糖激酶和异柠檬酸脱氢酶的活性,而姜黄暴露则没有明显(p<0.05)变化。此外,砒霜组和姜黄组在 180 天后都表现出 PPAR-α 表达下调。由于姜黄素具有很强的结合亲和力和多种氢键形式,因此通过分子内分析发现姜黄素是一种很有前景的抗动脉粥样硬化和砷相关疾病的成分。这些发现强调了姜黄对砷中毒的潜在治疗作用,为今后的研究和公共卫生干预提出了建议。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Turmeric as a therapeutic agent against arsenic-induced metabolic dysregulation in rat models

Ethnopharmacological relevance

Health hazards stemming from metalloid consumption, such as arsenic, pose a global concern. This study aimed to assess the protective effects of turmeric against arsenic-induced alterations in lipid profiles and energy metabolism in rats.

Methods

Thirty male rats were divided into three groups over a 90–180-day exposure period: Group 1 (Control) received standard rat chow; Group 2 received an arsenic diet; and Group 3 received arsenic plus turmeric supplemented diet. Blood and liver tissue samples were collected for lipid profiles, glucose levels, energy metabolism parameters, and PPAR-α mRNA expression using qRT-PCR. Statistical analysis was performed (p<0.05).

Results

Results indicated significant (p<0.05) increases in lipid profiles among arsenic-exposed rats after 180 days, elevating the risk of coronary artery diseases. Both arsenic and turmeric-exposed groups showed heightened total cholesterol (TC), triglycerides (TG), and low-density lipoprotein (LDL) levels at 90 and 180 days, with nuanced differences suggesting dyslipidemia and atherosclerosis. Blood glucose observations revealed hypoglycemia initially in arsenic-exposed rats, progressing to hyperglycemia by 180 days. Arsenic significantly (p<0.05) inhibited pyruvate kinase, hexokinase, and isocitrate dehydrogenase activities in the liver after 180 days, while turmeric exposure showed no significant (p<0.05) changes. Additionally, both arsenic and turmeric groups exhibited downregulation of PPAR-α expression at 180 days. In-silico analysis identified curcumin as a promising component for anti-atherosclerosis and arsenic-related conditions due to its strong binding affinities and multiple hydrogen bond formations.

Conclusion

In conclusion, long-term turmeric consumption may mitigate arsenic-induced oxidative damage associated with early hyperglycemia, diabetes mellitus, cardiovascular diseases, and atherosclerosis. These findings underscore turmeric’s potential therapeutic role against arsenic toxicity, suggesting avenues for future research and public health interventions.
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