Aim: This study aimed to investigate the protective effects of flavonoids from the stem and leaves of Scutellaria baicalensis Georgi (SSFs) against Aβ<sub>1-42</sub>-induced oligodendrocytes (OL) damage. ...Aim: This study aimed to investigate the protective effects of flavonoids from the stem and leaves of Scutellaria baicalensis Georgi (SSFs) against Aβ<sub>1-42</sub>-induced oligodendrocytes (OL) damage. Methods: Immunofluorescence was used for the detection of myelin-associated glycoprotein (MAG), a characteristic protein of rat oligodendrocytes (OLN-93 cells). To evaluate the potential protective effects of SSFs on OLN-93 cells injured by Aβ<sub>1-42</sub>, an injury model was established by subjecting OLN-93 cells to Aβ<sub>1-42</sub> exposed. Cell morphology was examined using an inverted microscope, while cell viability was assessed using the colorimetric method of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). Additionally, lactate dehydrogenase (LDH) was measured using the pyruvic acid reduction assay. The Ginkgo biloba leaf extract (GBE) injection was used as a positive control. Results: A total of >95% of the MAG immunofluorescence-positive cells were identified as oligodendrocytes. Gradually increasing concentrations of SSFs impaired the cells, and the maximum nondetrimental dose for OLN-93 cells was 75 mg/L. This study assessed the effects of SSFs on OLN-93 cells damaged by Aβ<sub>1-42</sub>. The results indicated that SSFs significantly improved OLN-93 cell morphological abnormal changes, increased the OLN-93 cell survival rate, and reduced LDH release. Conclusion: SSFs can alleviate Aβ<sub>1-42</sub>-induced damage of OL.展开更多
β－淀粉样蛋白（β－amyloid protein ，Aβ）在脑内的异常聚集在阿尔茨海默病（Alzheimer disease ，AD）的发生、发展中扮演着重要的角色。AD患者脑内Aβ代谢失衡，过量的Aβ蛋白会自发形成聚集体，引起神经细胞功能障碍、死亡，最...β－淀粉样蛋白（β－amyloid protein ，Aβ）在脑内的异常聚集在阿尔茨海默病（Alzheimer disease ，AD）的发生、发展中扮演着重要的角色。AD患者脑内Aβ代谢失衡，过量的Aβ蛋白会自发形成聚集体，引起神经细胞功能障碍、死亡，最终导致痴呆。目前研究显示Aβ聚集体主要为寡聚体，原纤维及纤维3种聚集形式，这3种聚集形式的构象不尽相同，对神经细胞造成的损伤方式也有所不同。进一步了解Aβ聚集体的分子结构，有助于对Aβ致病分子机制的认识，为以Aβ为靶点的AD抑制剂开发提供理论基础，本文针对最近关于Aβ聚集体分子结构的研究的前沿进展作一综述。展开更多
文摘Aim: This study aimed to investigate the protective effects of flavonoids from the stem and leaves of Scutellaria baicalensis Georgi (SSFs) against Aβ<sub>1-42</sub>-induced oligodendrocytes (OL) damage. Methods: Immunofluorescence was used for the detection of myelin-associated glycoprotein (MAG), a characteristic protein of rat oligodendrocytes (OLN-93 cells). To evaluate the potential protective effects of SSFs on OLN-93 cells injured by Aβ<sub>1-42</sub>, an injury model was established by subjecting OLN-93 cells to Aβ<sub>1-42</sub> exposed. Cell morphology was examined using an inverted microscope, while cell viability was assessed using the colorimetric method of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). Additionally, lactate dehydrogenase (LDH) was measured using the pyruvic acid reduction assay. The Ginkgo biloba leaf extract (GBE) injection was used as a positive control. Results: A total of >95% of the MAG immunofluorescence-positive cells were identified as oligodendrocytes. Gradually increasing concentrations of SSFs impaired the cells, and the maximum nondetrimental dose for OLN-93 cells was 75 mg/L. This study assessed the effects of SSFs on OLN-93 cells damaged by Aβ<sub>1-42</sub>. The results indicated that SSFs significantly improved OLN-93 cell morphological abnormal changes, increased the OLN-93 cell survival rate, and reduced LDH release. Conclusion: SSFs can alleviate Aβ<sub>1-42</sub>-induced damage of OL.
文摘β－淀粉样蛋白（β－amyloid protein ，Aβ）在脑内的异常聚集在阿尔茨海默病（Alzheimer disease ，AD）的发生、发展中扮演着重要的角色。AD患者脑内Aβ代谢失衡，过量的Aβ蛋白会自发形成聚集体，引起神经细胞功能障碍、死亡，最终导致痴呆。目前研究显示Aβ聚集体主要为寡聚体，原纤维及纤维3种聚集形式，这3种聚集形式的构象不尽相同，对神经细胞造成的损伤方式也有所不同。进一步了解Aβ聚集体的分子结构，有助于对Aβ致病分子机制的认识，为以Aβ为靶点的AD抑制剂开发提供理论基础，本文针对最近关于Aβ聚集体分子结构的研究的前沿进展作一综述。
