Abstract

Chronic D-galactose (D-gal) administration causes cognitive impairment and is used widely in animal models for anti-aging studies. Centella asiatica (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 Centella asiatica (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.

摘要

慢性 D-半乳糖 (D-gal) 给药会导致认知障碍，并广泛用于抗衰老研究的动物模型中。积雪草(CA) 是一种传统草药，已被用作大脑补品以增强记忆力。本研究评估积雪草乙醇提取物的神经保护作用(CAE) 对抗 D-gal 诱导的大鼠衰老。健康雄性大鼠分为三组：对照组、D-gal和D-gal + CAE。对照组接受生理盐水 (ip)，而 D-gal 组接受 D-gal (120 mg/kg bw, ip)，D-gal + CAE 组接受 D-gal (120 mg/kg bw, ip) ) 和 CAE (300 mg/kg bw, 口服) 每天 42 天。治疗后评估行为和脑生化和组织病理学变化。行为研究的结果表明，D-gal 显着降低了表明行为和认知障碍的自发交替和运动活动。生化研究表明，D-gal 显着增加大鼠脑中的氧化应激和乙酰胆碱酯酶活性 (AChE)。组织病理学研究表明，D-gal 扰乱了海马和皮质细胞的正常结构，表明这些脑区发生了退化。D-gal 和 CAE 联合治疗 42 天减轻了 D-gal 引起的行为、生化和神经解剖学损伤；它显着抑制大脑中 D-gal 诱导的氧化应激和 AChE 活性，并维持海马和皮质区域的正常细胞结构。因此，这项研究表明，CAE 可以通过调节 AChE 活性和氧化应激来保护大脑免受 D-gal 的不利影响（例如，记忆丧失和认知障碍）。它显着抑制大脑中 D-gal 诱导的氧化应激和 AChE 活性，并维持海马和皮质区域的正常细胞结构。因此，这项研究表明，CAE 可以通过调节 AChE 活性和氧化应激来保护大脑免受 D-gal 的不利影响（例如，记忆丧失和认知障碍）。它显着抑制大脑中 D-gal 诱导的氧化应激和 AChE 活性，并维持海马和皮质区域的正常细胞结构。因此，这项研究表明，CAE 可以通过调节 AChE 活性和氧化应激来保护大脑免受 D-gal 的不利影响（例如，记忆丧失和认知障碍）。