| Autor: |
Ren W; Department of Human Anatomy, Baotou Medical College, Inner Mongolia, China.; Key Laboratory of Human Anatomy, Education Department of Inner Mongolia Autonomous Region., Yan XS; Department of Human Anatomy, Baotou Medical College, Inner Mongolia, China.; Key Laboratory of Human Anatomy, Education Department of Inner Mongolia Autonomous Region., Fan JC; Department of Human Anatomy, Baotou Medical College, Inner Mongolia, China.; Key Laboratory of Human Anatomy, Education Department of Inner Mongolia Autonomous Region., Huo DS; Department of Human Anatomy, Baotou Medical College, Inner Mongolia, China.; Key Laboratory of Human Anatomy, Education Department of Inner Mongolia Autonomous Region., Wang XX; Key Laboratory of Human Anatomy, Education Department of Inner Mongolia Autonomous Region.; Department of pathology, Baotou Medical College, Inner Mongolia, China., Jia JX; Department of Human Anatomy, Baotou Medical College, Inner Mongolia, China.; Key Laboratory of Human Anatomy, Education Department of Inner Mongolia Autonomous Region., Yang ZJ; Key Laboratory of Human Anatomy, Education Department of Inner Mongolia Autonomous Region.; Department of Human Anatomy, Chifeng University, Inner Mongolia, China. |
| Abstrakt: |
One of the main pathological features noted in Alzheimer's disease (AD) is the presence of plagues of aggregated β-amyloid (Aβ1-42)-peptides. Excess deposition of amyloid-β oligomers (AβO) are known to promote neuroinflammation. Sequentially, following neuroinflammation astrocytes become activated with cellular characteristics to initiate activated astrocytes. The purpose of this study was to determine whether total flavonoids derived from Dracocephalum moldavica L . (TFDM) inhibited Aβ1-42-induced damage attributed to activated C8-D1A astrocytes. Western blotting and ELISA were used to determine the expression of glial fibrillary acidic protein (GFAP), and complement C3 to establish the activation status of astrocytes following induction from exposure to Aβ1-42. Data demonstrated that stimulation of C8-D1A astrocytes by treatment with 40 μM Aβ1-42 for 24 hr produced significant elevation in protein expression and protein levels of acidic protein (GFAP) and complement C3 accompanied by increased expression and levels of inflammatory cytokines. Treatment with TFDM or the clinically employed drug donepezil in AD therapy reduced production of inflammatory cytokines, and toxicity initiated following activation of C8-D1A astrocytes following exposure to Aβ1-42. Therefore, TFDM similar to donepezil inhibited inflammatory secretion in reactive astrocytes, suggesting that TFDM may be considered as a potential compound to be utilized in AD therapy. |
