Akgöl Jale, Kutlay Özden, Keskin Aktan Arzu, Fırat Fatma
Department of Medical Pharmacology, Faculty of Medicine, Afyonkarahisar Health Sciences University, 03030 Afyonkarahisar, Turkey.
Department of Physiology, Faculty of Medicine, Afyonkarahisar Health Sciences University, 03030 Afyonkarahisar, Turkey.
Curr Issues Mol Biol. 2024 Dec 11;46(12):13922-13936. doi: 10.3390/cimb46120832.
Modified citrus pectin (MCP) modulates galectin-3, a key player in neuroinflammation linked to Alzheimer's disease. By inhibiting galectin-3, MCP reduces the brain's inflammatory response and may alleviate cognitive decline. This study examines MCP's impact on neuroinflammation, cognitive function, and its role in galectin-3 inhibition in a dementia model. Male Wistar rats were assigned to four groups: control ( = 6), scopolamine (SCP) = 7), SCP + MCP ( = 7), and MCP only ( = 7). MCP was administered orally at 100 mg/kg/day via drinking water for six weeks. SCP was injected intraperitoneally at 1 mg/kg for seven days to induce an Alzheimer's-type dementia model. The researchers assessed cognitive performance through the Morris Water Maze (MWM) test. After behavioral tests, blood and brain tissues, including the hippocampus, were collected and stored at -80 °C for analysis. Immunohistochemistry was used to evaluate superoxide dismutase (SOD) activity, malondialdehyde (MDA) levels, brain-derived neurotrophic factor (BDNF), and inflammatory markers (IL-1β, IL-6, TNF-α, and galectin-3). The data were analyzed with SPSS 22. SCP treatment increased lipid peroxidation (MDA) and elevated inflammatory markers (TNF-α, IL-6, and galectin-3), while reducing BDNF and impairing spatial memory. Co-administering MCP with SCP significantly reduced TNF-α, IL-6, and galectin-3 levels; increased BDNF; and improved memory performance. Although MCP did not lower MDA levels, it boosted SOD activity, suggesting antioxidant effects. Modified citrus pectin (MCP) alleviated cognitive impairments and reduced neuroinflammation in Alzheimer's-type dementia by inhibiting galectin-3. MCP also exhibited antioxidant potential, underscoring its therapeutic promise for neurodegenerative diseases.
改性柑橘果胶（MCP）可调节半乳糖凝集素-3，后者是与阿尔茨海默病相关的神经炎症中的关键因子。通过抑制半乳糖凝集素-3，MCP可减轻大脑的炎症反应，并可能缓解认知衰退。本研究在痴呆模型中考察了MCP对神经炎症、认知功能的影响及其在抑制半乳糖凝集素-3中的作用。将雄性Wistar大鼠分为四组：对照组（n = 6）、东莨菪碱（SCP）组（n = 7）、SCP + MCP组（n = 7）和仅MCP组（n = 7）。MCP通过饮水以100 mg/kg/天的剂量口服给药六周。SCP以1 mg/kg的剂量腹腔注射七天以诱导阿尔茨海默病型痴呆模型。研究人员通过莫里斯水迷宫（MWM）试验评估认知表现。行为测试后，采集血液和包括海马体在内的脑组织，并储存在-80°C用于分析。采用免疫组织化学法评估超氧化物歧化酶（SOD）活性、丙二醛（MDA）水平、脑源性神经营养因子（BDNF）和炎症标志物（IL-1β、IL-6、TNF-α和半乳糖凝集素-3）。数据用SPSS 22进行分析。SCP处理增加了脂质过氧化（MDA）并升高了炎症标志物（TNF-α、IL-6和半乳糖凝集素-3），同时降低了BDNF并损害了空间记忆。MCP与SCP联合给药显著降低了TNF-α、IL-6和半乳糖凝集素-3水平；增加了BDNF；并改善了记忆表现。尽管MCP没有降低MDA水平，但它提高了SOD活性，表明具有抗氧化作用。改性柑橘果胶（MCP）通过抑制半乳糖凝集素-3减轻了阿尔茨海默病型痴呆中的认知障碍并减少了神经炎症。MCP还表现出抗氧化潜力，突出了其对神经退行性疾病的治疗前景。
