水飞蓟提取物复方水飞蓟宾对2型糖尿病大鼠及柴油机尾气颗粒(DEP)毒性的保护作用。

IF 4.8 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of Nutritional Biochemistry Pub Date : 2024-12-19 DOI:10.1016/j.jnutbio.2024.109836
Olamide Olusegun Awolaja
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引用次数: 0

摘要

柴油在发动机中的燃烧为大气中的柴油颗粒物质(DPM)贡献了多环芳烃,因此通过引发氧化调节引起毒性减轻后果。目前,据报道,2型糖尿病是一种全球性威胁,2019年造成约150万人死亡,占70岁以下人口相关死亡人数的48%左右。(GBDCN, 2020)。水飞蓟宾(silbinin, SIL)是一种从水飞蓟中提取的黄烷脂素,具有很强的治疗潜力。本研究阐明了SIL对DEP后糖尿病大鼠胰腺葡萄糖调节通路(PI3K-AKT-GLUT 2和AMPK-GLUT 2)、炎症和氧化还原失衡的影响。用链脲佐菌素诱导大鼠2型糖尿病,经40 mg/kg的SIL处理后,DEP(0.4和0.5 mg/kg)进一步危害大鼠。为了进行比较,平行组的非糖尿病大鼠暴露于DEP,然后用SIL治疗,同时将结果与糖尿病组进行比较。结果表明,SIL导致胰岛素相关基因(PI3K, AKT, AMPK, GLUT 2),炎症标志物(IL-1β, IL-10),过氧化(MDA, CD)和抗氧化状态(SOD, CAT, GPX, GSH, HO-1)在体内被DEP和高血糖负诱导的显著/实质性调节,从而恢复葡萄糖稳态。综上所述,SIL提供了改善DEP和高血糖/血糖水平升高引起的胰腺毒性的潜力。
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Protective potentials of extracted compound SILIBININ from milk thistle on type-2 diabetes mellitus and diesel exhaust particle (DEP) toxicity in experimental rats
The combustion of diesel in engines contributes polycyclic aromatic hydrocarbons to Diesel Particulate Matter (DPM) present in the atmosphere, therefore causing toxic mitigating consequences by eliciting oxidative modulation. Currently, type 2 diabetes mellitus is reported as a global menace, causing about 1.5 million deaths in 2019 and contributing to about 48% of related deaths among the populace aged below 70 years. (GBDCN, 2020). Silibinin (SIL) is a flavolignan from milk thistle with substantive therapeutic potential. This work elucidates the effects of SIL on glucose modulatory pathways (PI3K-AKT-GLUT 2 and AMPK-GLUT 2), inflammation and redox imbalance in the pancreas of diabetic rats subjected to DEP. Streptozocin was used to induce Type-2 diabetes mellitus in rats, which were further endangered to DEP (0.4 and 0.5 mg/kg) later, post-treated with SIL 40 mg/kg. For comparison, a parallel group of nondiabetic rats were exposed to DEP and afterwards treated with SIL, whilst the results were compared to the diabetic group. Results state that SIL leads to marked/substantial modulation in insulin-associated genes (PI3K, AKT, AMPK, GLUT 2), inflammatory markers (IL-1β, IL-10), peroxidation (MDA, CD) and antioxidative status (SOD, CAT, GPX, GSH, HO-1) in vivo as negatively induced by DEP and hyperglycaemia, thereby restoring glucose homeostasis. Taken together, SIL proffers the potential to ameliorate pancreatic-toxicity caused by DEP and high blood glucose/elevated glucose levels.
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来源期刊
Journal of Nutritional Biochemistry
Journal of Nutritional Biochemistry 医学-生化与分子生物学
CiteScore
9.50
自引率
3.60%
发文量
237
审稿时长
68 days
期刊介绍: Devoted to advancements in nutritional sciences, The Journal of Nutritional Biochemistry presents experimental nutrition research as it relates to: biochemistry, molecular biology, toxicology, or physiology. Rigorous reviews by an international editorial board of distinguished scientists ensure publication of the most current and key research being conducted in nutrition at the cellular, animal and human level. In addition to its monthly features of critical reviews and research articles, The Journal of Nutritional Biochemistry also periodically publishes emerging issues, experimental methods, and other types of articles.
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