Evaluation of Safety and Protective Effect of Combined Extract ofCissampelos pareiraandAnethum graveolens(PM52) against Age-Related Cognitive Impairment

Wipawee Thukham-mee,Jintanaporn Wattanathorn

doi:10.1155/2012/674101

Abstract

The present study aimed to determine acute toxicity, the protective effect, and underlying mechanism of PM52, a combined extract of Cissampelos pareira and Anethum graveolens, against age-related cognitive impairment in animal model of age-related cognitive impairment. PM52 was determined as acute toxicity according to OECD guideline. Male Wistar rats, weighing 180–220 g, were orally given PM52 at doses of 2, 10, and 50 mg/kg at a period of 14 days before and 7 days after the bilateral administration of AF64A via intracerebroventricular route. All animals were assessed according to spatial memory, neuron density, MDA level, the activities of SOD, CAT, GSH-Px, and AChEI effect in hippocampus. It was found that all doses of PM52 could attenuate memory impairment and neurodegeneration in hippocampus. The possible mechanisms might occur via the suppression of AChE and the decreased oxidative stress in hippocampus. Therefore, our data suggest that PM52 may serve as food supplement to protect against age-related cognitive impairment such as mild cognitive impairment (MCI) and early phase of Alzheimer's disease. However, further researches are still essential.

Highlights

Aging is a phenomenon leading to the dysfunction of normal cellular regulation including cognitive function
Current studies demonstrate that cognitive impairment in both aged human and rodents is correlated with the accumulation of oxidative damage to lipids, proteins, nucleic acids [1,2,3], and the vulnerability of various neurotransmitters to oxidative stress [4,5,6]
Based on the role of oxidative stress and cholinergic system mentioned earlier, it has provided the rationale for protecting and treating agerelated cognitive decline with substances targeting at enhancing cholinergic function and decreasing oxidative stress

Summary

Introduction

Aging is a phenomenon leading to the dysfunction of normal cellular regulation including cognitive function. Age-related cognitive memory impairment is one of the important health problems that should be concerned. Current studies demonstrate that cognitive impairment in both aged human and rodents is correlated with the accumulation of oxidative damage to lipids, proteins, nucleic acids [1,2,3], and the vulnerability of various neurotransmitters to oxidative stress [4,5,6]. Since the present strategy has not yet been met by effective symptomatic treatments or preventative strategies, the novel strategy to protect against age-related cognitive decline is still required. Based on the role of oxidative stress and cholinergic system mentioned earlier, it has provided the rationale for protecting and treating agerelated cognitive decline with substances targeting at enhancing cholinergic function and decreasing oxidative stress

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Discussion

Conclusion