Gossypium herbaceam Extracts Inhibited NF-κB Activation to Attenuate Spatial Memory Impairment and Hippocampal Neurodegeneration Induced by Amyloid-β in Rats
Affiliations: [a] School of Basic Medicine, Peking Union Medical College & Institute of Basic Medical Science, Chinese Academy of Medical Sciences, Beijing, China | [b] Xinjiang Technical Institute of Physics and Chemistry, Chinese Academy of Sciences, Urumqi, China | [c] Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
Correspondence:
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Corresponding authors: Ping-Ping Zuo, PhD, Department of Pharmacology, School of Basic Medicine, Peking Union Medical College & Institute of Basic Medical Science, Chinese Academy of Medical Sciences, 5 Dong Dan San Tiao, District Dongcheng, Beijing 100005, China. Tel./Fax: +86 10 6529 6404; E-mail: pingping_zuo@126.com. Hai-Bo Zhu, PhD, Key Laboratory of Bioactive Substances and Resources Utilization of Chinese Herbal Medicine affiliated Ministry of Education, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, 1 Road Xian Nong Tan, District Xuanwu, Beijing 100050, China. Tel./Fax: +86 10 6318 8106; E-mail: zhuhaibo@imm.ac.cn.
Note: [1] Chao Ji and Haji Akber Aisa contributed equally to this work.
Abstract: Amyloid-β (Aβ) is considered to be responsible for the pathogenesis of Alzheimer's disease. In the present study, the protective effect of Gossypium herbaceam extracts (GHE) on learning and memory impairment induced by Aβ were examined in vivo using Morris water maze and step through task. Furthermore, the antioxidant activity and neuroprotective effect of GHE was investigated with methods of histochemistry and biochemistry. These data showed that oral administration with GHE at the doses of 35, 70 and 140 mg/kg exerted an improved effect on the learning and memory impairment in rats induced by intracerebroventricular (i.c.v.) injection of 10 μg of Aβ25–35. Subsequently, the GHE afforded a beneficial action on promotion on the activity of glutathione peroxidase and catalase, as well as inhibition on the NF-κB activation in the hippocampus followed by the presence of Aβ25–35. Meanwhile, the number of degenerating neurons with an apoptotic feature was dramatically decreased in hippocampus after treatment with GHE, implicating that its antioxidant stress and inhibition of NF-κB activation could be involved in the mechanism underlying neuroprotection of GHE against Aβ-induced cell death. These findings suggested that GHE might be a potential agent for treatment of Alzheimer's disease.
