Department of Medicinal Chemistry, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India.
Department of Pathology, MSR Medical College, Bengaluru, India.
Drug Chem Toxicol. 2022 May;45(3):1417-1426. doi: 10.1080/01480545.2020.1833907. Epub 2020 Oct 20.
Chronic D-galactose (D-gal) administration causes cognitive impairment and is used widely in animal models for anti-aging studies. (CA), a traditional herbal medicine, has been used as a brain tonic to enhance memory. This study evaluates the neuroprotective role of an ethanolic extract of (CAE) against D-gal-induced aging in rats. Healthy male rats were divided into three groups: Control, D-gal, and D-gal + CAE. The Control group received normal saline (i.p.), whereas the D-gal group received D-gal (120 mg/kg b.w., i.p.), and the D-gal + CAE group received D-gal (120 mg/kg b.w., i.p.) and CAE (300 mg/kg b.w., orally) daily for 42 days. Behavioral and brain biochemical and histopathological changes were assessed after treatment. The results of the behavioral study depicted that D-gal significantly reduces the spontaneous alternation and locomotor activity indicating behavioral and cognitive impairment. Biochemical studies showed that D-gal significantly increases the oxidative stress and acetylcholinesterase activity (AChE) in rat brain. Histopathological study showed that D-gal disturbs the normal architecture of hippocampal and cortical cells, indicating degeneration in these brain areas. D-gal and CAE co-treatment for 42 days attenuated the behavioral, biochemical, and neuroanatomical impairments caused by the D-gal; it markedly suppresses the D-gal-induced oxidative stress and AChE activity in the brain, and maintains the normal cellular architecture in hippocampal and cortical areas. Thus, this study shows that CAE can protect the brain from the adverse effects of D-gal (e.g., memory loss and cognitive impairment) by modulating AChE activity and oxidative stress.
慢性 D-半乳糖（D-gal）给药会导致认知障碍，并且被广泛用于抗衰老研究的动物模型中。（CA），一种传统的草药，已被用作补脑剂以增强记忆力。本研究评估了（CAE）的乙醇提取物对 D-gal 诱导的大鼠衰老的神经保护作用。健康雄性大鼠分为三组：对照组、D-gal 组和 D-gal+CAE 组。对照组给予生理盐水（ip），D-gal 组给予 D-gal（120mg/kg b.w.，ip），D-gal+CAE 组给予 D-gal（120mg/kg b.w.，ip）和 CAE（300mg/kg b.w.，口服），每天一次，共 42 天。治疗后评估行为和大脑生化及组织病理学变化。行为研究结果表明，D-gal 显著降低自发交替和运动活性，表明行为和认知障碍。生化研究表明，D-gal 显著增加大鼠大脑中的氧化应激和乙酰胆碱酯酶（AChE）活性。组织病理学研究表明，D-gal 扰乱海马和皮质细胞的正常结构，表明这些大脑区域发生退化。D-gal 和 CAE 共同治疗 42 天可减轻 D-gal 引起的行为、生化和神经解剖学损伤；它显著抑制 D-gal 诱导的大脑中的氧化应激和 AChE 活性，并维持海马和皮质区域的正常细胞结构。因此，本研究表明 CAE 可以通过调节 AChE 活性和氧化应激来保护大脑免受 D-gal（例如，记忆力丧失和认知障碍）的不良影响。
