Chrysin mitigates neuronal apoptosis and impaired hippocampal neurogenesis in male rats subjected to D-galactose-induced brain aging.

IF 4.4 4区 医学 Q1 GERIATRICS & GERONTOLOGY
Biogerontology Pub Date : 2024-11-01 Epub Date: 2024-09-19 DOI:10.1007/s10522-024-10140-8
Ram Prajit, Rasa Saenno, Kornrawee Suwannakot, Soraya Kaewngam, Tanaporn Anosri, Nataya Sritawan, Anusara Aranarochana, Apiwat Sirichoat, Wanassanun Pannangrong, Peter Wigmore, Jariya Umka Welbat
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引用次数: 0

Abstract

Oxidative stress-induced neuronal apoptosis is primarily involved in brain aging and impaired hippocampal neurogenesis. Long-term D-galactose administration increases oxidative stress related to brain aging. Chrysin, a subtype of flavonoids, exhibits neuroprotective effects, particularly its antioxidant properties. To elucidate the neuroprotection of chrysin on neuronal apoptosis and an impaired hippocampal neurogenesis relevant to oxidative damage in D-galactose-induced brain aging, male Sprague Dawley rats were allocated into vehicle control, D-galactose, chrysin, and cotreated rats. The rats received their respective treatments daily for 8 weeks. The reactions of scavenging enzymes, protein regulating endogenous antioxidant defense, and anti-apoptotic protein expression were significantly reduced in the hippocampus and prefrontal cortex of the animals receiving D-galactose. Conversely, product of oxidative damage and apoptotic protein expressions were significantly elevated in both cortical areas of the D-galactose group. In hippocampal neurogenesis, significant upregulation of cell cycle arrest and decrease in differentiated protein expression were detected after D-galactose administration. Nevertheless, chrysin supplementation significantly mitigated all negative effects in animals receiving D-galactose. This study demonstrates that chrysin likely attenuates brain aging induced by D-galactose by enhancing scavenging enzyme activities and reducing oxidative stress, neuronal apoptosis, and the impaired hippocampal neurogenesis.

蛹虫草苷可减轻D-半乳糖诱导的雄性大鼠脑衰老过程中神经元凋亡和海马神经发生受损的程度
氧化应激诱导的神经细胞凋亡主要与大脑衰老和海马神经发生受损有关。长期服用 D-半乳糖会增加与大脑衰老有关的氧化应激。菊黄素是黄酮类化合物的一种亚型,具有神经保护作用,尤其是其抗氧化特性。为了阐明菊黄素对神经元凋亡的神经保护作用,以及菊黄素在 D-半乳糖诱导的脑衰老中与氧化损伤相关的海马神经发生受损的作用,研究人员将雄性 Sprague Dawley 大鼠分为药物对照组、D-半乳糖组、菊黄素组和共处理组。大鼠每天分别接受相应的处理,持续 8 周。结果表明,服用D-半乳糖的大鼠海马和前额叶皮质中清除酶的反应、调节内源性抗氧化防御的蛋白质和抗凋亡蛋白质的表达均明显减少。相反,氧化损伤产物和凋亡蛋白的表达在D-半乳糖组动物的两个皮层区域都明显升高。在海马神经发生中,服用 D-半乳糖后发现细胞周期停滞明显上调,分化蛋白表达减少。然而,补充菊粉能明显减轻D-半乳糖对动物的所有负面影响。这项研究表明,菊粉可能通过增强清除酶活性、减少氧化应激、神经细胞凋亡和海马神经发生受损来减轻D-半乳糖诱导的脑衰老。
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来源期刊
Biogerontology
Biogerontology 医学-老年医学
CiteScore
8.00
自引率
4.40%
发文量
54
审稿时长
>12 weeks
期刊介绍: The journal Biogerontology offers a platform for research which aims primarily at achieving healthy old age accompanied by improved longevity. The focus is on efforts to understand, prevent, cure or minimize age-related impairments. Biogerontology provides a peer-reviewed forum for publishing original research data, new ideas and discussions on modulating the aging process by physical, chemical and biological means, including transgenic and knockout organisms; cell culture systems to develop new approaches and health care products for maintaining or recovering the lost biochemical functions; immunology, autoimmunity and infection in aging; vertebrates, invertebrates, micro-organisms and plants for experimental studies on genetic determinants of aging and longevity; biodemography and theoretical models linking aging and survival kinetics.
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