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] These authors contributed equally to this work.
Abstract: Excitotoxicity is one of the most extensively studied processes of neuronal death and plays an important role in Alzheimer's disease. In the present study, the protective effects of Gossypium herbaceam extracts (GHE) on learning and memory impairment induced by excitatory neurotoxin ibotenic acid were examined in vivo using Morris water maze. Furthermore, neuroprotective effects of GHE were investigated with methods of immunohistochemistry and biochemistry. Our 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 intracerebral injection of ibotenic acid. To confirm the precise mechanism of memory improvement by presence of GHE, we further investigated the potential protection on the hippocampus. Our findings suggest that GHE afforded a beneficial inhibition on pro-apoptosis proteins expression following ibotenic acid. Additionally, calcium pump activity and calbindin-D28k expression were dramatically increased after GHE treatment, implicating that the modulation of calcium homeostasis could be involved in the mechanism underlying neuroprotection of GHE against ibotenic acid-induced excitotoxicity. These data suggested that GHE could be a potential agent for preventing or retarding the development or progression of Alzheimer's disease.
