Planta Med 2011; 77(18): 1977-1983
DOI: 10.1055/s-0031-1280125
Biological and Pharmacological Activity
Original Papers
© Georg Thieme Verlag KG Stuttgart · New York

Uncaria rhynchophylla Ameliorates Cognitive Deficits Induced by D-galactose in Mice

Yan-Fang Xian1 , Zhi-Xiu Lin1 , Ming Zhao1 , Qing-Qiu Mao1 , Siu-Po Ip1 , Chun-Tao Che1 , 2
  • 1School of Chinese Medicine, The Chinese University of Hong Kong, Shatin, N. T., Hong Kong SAR, China
  • 2Department of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, University of Illinois at Chicago, Chicago, Illinois, USA
Further Information

Publication History

received February 28, 2011 revised June 24, 2011

accepted July 1, 2011

Publication Date:
19 August 2011 (online)

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Abstract

The stem with hooks of Uncaria rhynchophylla is a component herb of many traditional formulae for the treatment of neurodegenerative diseases. However, scientific evidence of the efficacy of Uncaria rhynchophylla in the treatment of Alzheimer's disease (AD) in animal models is lacking. Thus, in the present study, we investigated whether the 70 % aqueous ethanol extract of Uncaria rhynchophylla (EUR) could protect against D-galactose (D-gal)-induced cognitive deficits in mice. Mice were given a subcutaneous injection of D-gal (50 mg/kg) and orally administered EUR (100, 200, or 400 mg/kg) daily for 8 weeks. The effect of EUR on D-gal-induced cognitive deficits was evaluated by measuring behavioral and neurochemical parameters of AD and the antioxidant status of brain tissue. The results showed that EUR (200 or 400 mg/kg) significantly increased exploratory behavior (assessed by an open-field test) and improved spatial learning and memory function (assessed by the Morris water maze test) in D-gal-treated mice. In addition, EUR (200 or 400 mg/kg) significantly increased the levels of acetylcholine and glutathione and decreased the activity of acetylcholinesterase and the level of malondialdehyde in the brains of D-gal-treated mice. These results indicate that EUR ameliorates cognitive deficits induced by D-gal in mice, and that this action may be mediated, at least in part, by the inhibition of acetylcholinesterase activity and the enhancement of the antioxidant status of brain tissue.

References

Dr. Siu-Po Ip

School of Chinese Medicine
The Chinese University of Hong Kong

Shatin, Hong Kong

China

Phone: +852 31 63 44 57

Fax: +852 31 63 44 59

Email: paulip@cuhk.edu.hk