Chrysin alleviates the impeded neurogenesis in accelerated brain aging by D-galactose in rats.

IF 4.4 4区 医学 Q1 GERIATRICS & GERONTOLOGY Biogerontology Pub Date : 2025-03-14 DOI:10.1007/s10522-025-10215-0
Ram Prajit, Nataya Sritawan, Anusara Aranarochana, Apiwat Sirichoat, Wanassanun Pannangrong, Peter Wigmore, Jariya Umka Welbat
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Abstract

Aged-related cognitive impairments are associated with molecular neurodegenerations and impeded neurogenesis in the dentate gyrus (DG) of the damaged hippocampus. Neurogenesis requires activated cyclic AMP-responsive element-binding protein (CREB) pathway to enhance neuronal development, synaptic plasticity, cognition, learning and memory. Current research has reported that consecutive administration of D-galactose can accelerate brain aging by inducing oxidation and inflammation. The flavonoid chrysin has been demonstrated in medical dietary supplements and shown neuroprotective effect on impeded neurogenesis. This study aimed to clarify that chrysin preserves neurogenesis by modulating molecular pathway in accelerated brain aging induced by D-galactose. Signs of aging, processes of neurogenesis, and protein regulating neurogenesis were evaluated in male Sprague Dawley (SD) rats, which were allocated into four groups: vehicle rats, accelerated aging rats treated with D-galactose, normal rats receiving chrysin, and cotreated rats receiving both D-galactose and chrysin. Aging signs showed only a subsidence in volume of the granular cell layer (GCL) after consecutive administration of D-galactose. Cell proliferation, neurogenic niches, and protein regulating proliferation were downregulated in the accelerated aging rats. Likewise, cell survivals and proteins related to CREB pathway were depleted in rats receiving D-galactose. Nevertheless, rats cotreated with chrysin maintained in all parameters that were adversely affected by D-galactose. In conclusion, chrysin could alleviate the disruption of molecular regulation of neurogenesis in accelerated brain aging induced by D-galactose.

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蛹虫草素能缓解 D-半乳糖加速大鼠脑衰老过程中的神经发生障碍。
与年龄相关的认知障碍与分子神经变性和受损海马齿状回(DG)的神经发生受阻有关。神经发生需要激活环磷酸腺苷反应元件结合蛋白(CREB)通路,以促进神经元发育、突触可塑性、认知、学习和记忆。目前的研究报告显示,连续服用 D-半乳糖会诱发氧化和炎症,从而加速大脑衰老。医学膳食补充剂中的黄酮类化合物金丝桃素已被证实对神经发生受阻具有神经保护作用。本研究旨在阐明,在 D-半乳糖诱导的加速脑衰老过程中,菊黄素可通过调节分子通路来保护神经发生。研究人员将雄性Sprague Dawley(SD)大鼠分为四组,分别为载体大鼠组、用D-半乳糖治疗的加速衰老大鼠组、接受金黄素治疗的正常大鼠组和接受D-半乳糖和金黄素共同治疗的大鼠组,对其衰老迹象、神经发生过程和调节神经发生的蛋白质进行了评估。在连续服用 D-半乳糖后,衰老迹象仅表现为颗粒细胞层(GCL)的体积缩小。在加速衰老的大鼠体内,细胞增殖、神经源龛和调节增殖的蛋白质都出现了下调。同样,服用 D-半乳糖的大鼠体内细胞存活率和与 CREB 通路相关的蛋白质也会减少。然而,与菊黄素共同处理的大鼠在所有受 D-半乳糖不利影响的参数上都保持不变。总之,金黄素可以缓解 D-半乳糖对加速脑衰老的神经发生的分子调控的破坏。
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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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