Zhang Shu-Feng, Dong Yong-Cai, Zhang Xiao-Feng, Wu Xiao-Guang, Cheng Jian-Jun, Guan Li-Hua, Shang Ya-Zhen
a Hebei Province Key Research Office of Traditional Chinese Medicine Against Dementia, Institute of Traditional Chinese Medicine, Chengde Medical College, Hebei Province Key Laboratory of Traditional Chinese Medicine Research and Development , Chengde , Hebei , PR China and.
b Workers Hospital of Chengde Iron & Steel Group Co., Ltd , Chengde , Hebei , PR China.
Brain Inj. 2015;29(11):1376-82. doi: 10.3109/02699052.2015.1042053. Epub 2015 Jun 17.
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.
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 β-amyloid peptide 1-40 (Aβ1-40) 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.
The results showed that OA-treated rats exhibited marked neuronal damage accompanied by increased levels of Aβ1-40 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.
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 Aβ expression in the treatment of Alzheimer's disease.
研究从黄芩地上部分分离得到的黄酮类化合物(SSF)对大鼠冈田酸(OA)诱导的脑损伤的影响。
以200 ng kg⁻¹的剂量将OA微量注射到雄性大鼠的右侧脑室,注射两次,间隔3天,以建立类似阿尔茨海默病的脑损伤模型。用硫堇染色观察神经元形态,通过免疫组织化学监测胶质纤维酸性蛋白(GFAP)和β-淀粉样肽1-40(Aβ1-40)的表达。采用分光光度法测定丙二醛(MDA)水平、谷胱甘肽过氧化物酶(GSH-Px)和乳酸脱氢酶(LDH)活性。
结果表明,OA处理的大鼠表现出明显的神经元损伤,伴有Aβ1-40肽水平升高和MDA积累、GFAP蛋白表达降低以及脑中GSH-Px和LDH活性降低。三种剂量(25、50和100 mg kg⁻¹)的SSF显著逆转了OA诱导的大鼠脑内变化。
SSF介导改善OA诱导的大鼠神经元损伤,为评估SSF作为减少tau过度磷酸化和Aβ表达以治疗阿尔茨海默病的手段提供了理论依据。