Neuroprotective Effects of Carnosic Acid in an Experimental Model of Alzheimer’s Disease in Rats


Nahid Azad, M.Sc., 1Homa Rasoolijazi, Ph.D., 2,*Mohammad Taghi Joghataie, Ph.D., 1Sara Soleimani, M.Sc., 2
1. Cellular and Molecular Research Center, Tehran University of Medical Sciences (Hemmat Pardis), Tehran, Iran
2. Anatomy Department, School of Medicine, Tehran University of Medical Sciences (Hemmat Pardis), Tehran, Iran
1. Cellular and Molecular Research Center, Tehran University of Medical Sciences (Hemmat Pardis), Tehran, Iran
2. Anatomy Department, School of Medicine, Tehran University of Medical Sciences (Hemmat Pardis), Tehran, Iran
* Corresponding Address: Anatomy Department School of Medicine Tehran University of Medical Sciences (Hemmat Pardis) TehranIran Email:homa.rasooli@gmail.com
Any use, distribution, reproduction or abstract of this publication in any medium, with the exception of commercial purposes, is permitted provided the original work is properly cited This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Azad Nahid, Rasoolijazi Homa, Joghataie Mohammad Taghi, Soleimani Sara. Neuroprotective Effects of Carnosic Acid in an Experimental Model of Alzheimer’s Disease in Rats. Cell J. 2011; 13(1): 39-44.

Abstract

Objective:

Alzheimer’s disease is the most common type of neurodegenerative disorder. It has been suggested that oxidative stress can be one of the pathological mechanisms of this disease. Carnosic acid (CA) is an effective antioxidant substance and recent studies have shown that its electrophilic compounds play a role in reversing oxidative stress. Thus we tried to find out whether CA administration protects hippocampal neurons, preventing neurodegeneration in rats.

Materials and Methods:

Animals were divided into four groups: Sham-operated (sham), CA-pretreated sham-operated (sham+CA), untreated lesion (lesion) and CA-pretreated lesion (lesion+CA). Animals in all groups received vehicle or vehicle plus CA (CA: 10mg/ kg) intra-peritoneally one hour before surgery, again the same solution injected 3-4 hours after surgery (CA: 3 mg/kg) and repeated each afternoon for 12 days. A lesion was made by bilateral intra-hippocampal injection of 4 µl of beta amyloid protein (1.5 nmol/µl) or vehicle in each side. 14 days after surgery, the brains were extracted for histochemical studies. Data was expressed as mean ± SEM and analyzed using SPSS statistical software.

Results:

Results showed that pretreatment with carnosic acid can reduce cellular death in the cornu ammonis 1 (CA1) region of the hippocampus in the lesion+CA group, as compared with the lesion group.

Conclusion:

Carnosic acid may be useful in protecting against beta amyloid-induced neurodegeneration in the hippocampus.