Hebei University of Chinese Medicine, Shijiazhuang, China.
Hebei University of Chinese Medicine, Shijiazhuang, China; Hebei Key Laboratory of Chinese Medicine Research on Cardio-cerebrovascular Disease, Shijiazhuang, China.
Arch Med Res. 2022 Jan;53(1):20-28. doi: 10.1016/j.arcmed.2021.05.005. Epub 2021 Jul 1.
We investigated the effects of astragaloside IV (AS-IV) on memory function in aging rats mimicked by D-galactose administration and explored the potential molecular mechanisms.
Twenty-seven male rats were randomly divided into control group (N = 9), model group (N = 9), and AS-IV treated group (N = 9). Aging model was stimulated by D-galactose (400 mg/kg/d, i.p., dissolved in saline) for 8 weeks in rats. The general status of the rats was observed weekly. Learning and memory function was determined using the eight-arm radical maze and step-down test. Pathological changes in the hippocampal CA1 region were determined by hematoxylin and eosin staining. Organ indexes, superoxide dismutase (SOD) activity and malonaldehyde (MDA) content in the serum were measured. Expression of advanced glycation end products (AGEs), receptor for AGEs (RAGE), nuclear factor-κB (NF-κB), interleukin (IL)-6, IL-1β and tumor necrosis factor-α (TNF-α) were detected by enzyme-linked immunosorbent assay, real-time polymerase chain reaction or western blotting.
AS-IV improved the general status of the aging rats induced by D-galactose, prevented the impairment of memory function, organ indexes, and the pathological damage of the hippocampus. From the prospective of oxidative stress, AS-IV increased sera SOD activity and decreased MDA content. Additionally, AS-IV also reduced the inflammatory response by reducing hippocampal IL-1β, TNF-α, and IL-6 expression. Importantly, AS-IV prevented D-galactose-induced expression of AGEs, RAGE and NF-κB in the hippocampus.
AS-IV could prevent D-galactose-induced aging and memory impairment in rats, likely via regulation of inflammatory response, which was modulated by AGEs/RAGE/NF-κB axis.
我们研究了黄芪甲苷（AS-IV）对 D-半乳糖诱导衰老大鼠记忆功能的影响，并探讨了其潜在的分子机制。
将 27 只雄性大鼠随机分为对照组（N=9）、模型组（N=9）和 AS-IV 治疗组（N=9）。大鼠腹腔注射 D-半乳糖（400 mg/kg/d，溶于生理盐水）8 周，建立衰老模型。每周观察大鼠一般状态。采用八臂迷津和避台试验检测大鼠学习记忆功能。苏木精-伊红（HE）染色观察海马 CA1 区病理改变。酶联免疫吸附试验、实时聚合酶链反应或免疫印迹法检测血清中超氧化物歧化酶（SOD）活性和丙二醛（MDA）含量、晚期糖基化终产物（AGEs）、AGEs 受体（RAGE）、核因子-κB（NF-κB）、白细胞介素（IL）-6、IL-1β和肿瘤坏死因子-α（TNF-α）的表达。
AS-IV 改善了 D-半乳糖诱导衰老大鼠的一般状态，防止了记忆功能、器官指数和海马病理损伤的损害。从氧化应激的角度来看，AS-IV 增加了血清 SOD 活性，降低了 MDA 含量。此外，AS-IV 还通过降低海马 IL-1β、TNF-α和 IL-6 的表达来减轻炎症反应。重要的是，AS-IV 还可防止 D-半乳糖诱导的海马 AGEs、RAGE 和 NF-κB 的表达。
AS-IV 可预防 D-半乳糖诱导的大鼠衰老和记忆障碍，可能通过调节 AGEs/RAGE/NF-κB 轴来调节炎症反应。
