Flavonoids from Scutellaria attenuate okadaic acid-induced neuronal damage in rats

被引:15
作者
Zhang, Shu-Feng [1 ]
Dong, Yong-Cai [1 ,2 ]
Zhang, Xiao-Feng [1 ]
Wu, Xiao-Guang [1 ]
Cheng, Jian-Jun [1 ]
Guan, Li-Hua [1 ]
Shang, Ya-Zhen [1 ]
机构
[1] Chengde Med Coll, Inst Tradit Chinese Med, Hebei Prov Key Res Off Tradit Chinese Med Dementi, Hebei Prov Key Lab Tradit Chinese Med Res & Dev, Chengde, Hebei, Peoples R China
[2] Chengde Iron & Steel Grp Co Ltd, Workers Hosp, Chengde, Hebei, Peoples R China
关键词
A beta 1-40; astrocyte; GSH-Px; LDH; MDA; okadaic acid; neuropathology; SSF; BAICALENSIS GEORGI; MEMORY IMPAIRMENT; OXIDATIVE STRESS; TAU; PHOSPHATASES; DYSFUNCTION; PREVENTION; PATHOLOGY; INJURY; LEAVES;
D O I
10.3109/02699052.2015.1042053
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Primary objective: To study the effect of flavonoids isolated from aerial parts of Scutellaria baicalensis Georgi (SSF) on cerebral damage induced by okadaic acid (OA) in rats. Methods and procedures: OA was microinjected into the right lateral ventricle of male rats at a dose of 200 ng kg(-1) twice with a 3-day interval between injections to establish a model of Alzheimer's-disease-like cerebral damage. Neuronal morphology was observed with thionin staining and the expressions of glial fibrillary acidic protein (GFAP) and b-amyloid peptide 1-40 (Ab1-40) were monitored via immunohistochemistry. The level of malondialdehyde (MDA) and the activities of glutathione peroxidase (GSH-Px) and lactate dehydrogenase (LDH) were measured using spectrophotometry. Main outcomes and results: The results showed that OA-treated rats exhibited marked neuronal damage accompanied by increased levels of Ab1-40 peptide and MDA accumulation, decreased GFAP protein expression and reduced GSH-Px and LDH activity in the brain. SSF at three doses (25, 50 and 100 mg kg(-1)) dramatically reversed the OA-induced changes in the brains of rats. Conclusion: SSF-mediated amelioration of OA-induced neuronal damage in rats provides a rationale for assessing SSF as a means of to reducing tau hyperphosphorylation and Ab expression in the treatment of Alzheimer's disease.
引用
收藏
页码:1376 / 1382
页数:7
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