Neuroprotective effects of Tanshinone IIA in an acrylamide-induced in-vivo zebrafish model: Behavioral, biochemical and molecular restoration

IF 2.5 4区 生物学 Q1 ANATOMY & MORPHOLOGY
Gokul Sudhakaran , S. Madesh , V.N. Dhaareshwar , Mikhlid H. Almutairi , Bader O. Almutairi , Sungkwon Park , Jesu Arockiaraj
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Abstract

Acrylamide is a neurotoxic chemical widely present in carbohydrate-rich foods due to thermal processing. Chronic exposure to acrylamide can lead to oxidative stress, neuroinflammation, and neurodegeneration, resulting in motor dysfunction and cognitive impairments. In this study, we evaluated the neuroprotective potential of Tanshinone IIA (TIIA), a bioactive compound derived from Salvia miltiorrhiza (Danshen), on an adult zebrafish model induced with acrylamide. Zebrafish were exposed to acrylamide to induce neurotoxic stress, followed by treatment with varying concentrations of TIIA. Our results highlight that TIIA significantly improved survival rates and restored behavioral deficits caused by acrylamide, including impaired exploratory behavior and increased anxiety-like responses. Biochemically, TIIA restored antioxidant enzyme activities such as superoxide dismutase (SOD) and catalase (CAT), which were reduced by acrylamide exposure, thereby mitigating oxidative stress. TIIA also decreased lactate dehydrogenase (LDH) activity, indicative of reduced cellular damage, and restored acetylcholinesterase (AChE) activity, crucial for cholinergic neurotransmission. At the molecular level, TIIA reduced the activity of pro-inflammatory genes by stopping transcription, which acrylamide had increased, and brought the levels of neuroprotective genes like bdnf and nrf back to normal. Additionally, histological investigation showed that TIIA treatment significantly restored the morphological damage caused by acrylamide in the brain tissue of zebrafish. We draw conclusions on TIIA's neuroprotective effectiveness against acrylamide-induced neurotoxicity, demonstrating its potential as a treatment to stop acrylamide processed foods from causing neurodegenerative diseases.
丹参酮IIA在丙烯酰胺诱导的斑马鱼体内模型中的神经保护作用:行为、生化和分子修复
丙烯酰胺是一种神经毒性化学物质,由于热加工而广泛存在于富含碳水化合物的食物中。长期接触丙烯酰胺会导致氧化应激、神经炎症和神经变性,导致运动功能障碍和认知障碍。在这项研究中,我们评估了丹参酮IIA (TIIA),一种从丹参中提取的生物活性化合物,对丙烯酰胺诱导的成年斑马鱼模型的神经保护作用。将斑马鱼暴露于丙烯酰胺诱导神经毒性应激,然后用不同浓度的TIIA处理。我们的研究结果强调,TIIA显著提高了存活率,并恢复了丙烯酰胺引起的行为缺陷,包括受损的探索行为和增加的焦虑样反应。生物化学上,TIIA恢复了丙烯酰胺暴露导致的超氧化物歧化酶(SOD)和过氧化氢酶(CAT)等抗氧化酶活性,从而减轻了氧化应激。TIIA还降低了乳酸脱氢酶(LDH)活性,表明细胞损伤减轻,并恢复了乙酰胆碱酯酶(AChE)活性,这是胆碱能神经传递的关键。在分子水平上,TIIA通过阻止丙烯酰胺增加的转录来降低促炎基因的活性,并使bdnf和nrf等神经保护基因的水平恢复正常。此外,组织学研究表明,TIIA处理能显著恢复丙烯酰胺引起的斑马鱼脑组织形态学损伤。我们得出结论,TIIA对丙烯酰胺诱导的神经毒性具有神经保护作用,表明其有潜力阻止丙烯酰胺加工食品引起神经退行性疾病。
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来源期刊
Tissue & cell
Tissue & cell 医学-解剖学与形态学
CiteScore
3.90
自引率
0.00%
发文量
234
期刊介绍: Tissue and Cell is devoted to original research on the organization of cells, subcellular and extracellular components at all levels, including the grouping and interrelations of cells in tissues and organs. The journal encourages submission of ultrastructural studies that provide novel insights into structure, function and physiology of cells and tissues, in health and disease. Bioengineering and stem cells studies focused on the description of morphological and/or histological data are also welcomed. Studies investigating the effect of compounds and/or substances on structure of cells and tissues are generally outside the scope of this journal. For consideration, studies should contain a clear rationale on the use of (a) given substance(s), have a compelling morphological and structural focus and present novel incremental findings from previous literature.
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