Oral administration of avocado soybean unsaponifiables (ASU) reduces ischemic damage in the rat hippocampus.
BACKGROUND
The beneficial effects of avocado/soybean unsaponifiables (ASU) are known as an antiarthritic agent. This experimental study presents the effects of ASU on oxidant/antioxidant systems and the number of apoptotic neurons of hippocampal formation after ischemia and reperfusion.


METHODS
Eighteen rats were divided into three equal groups: group I rats were used as controls; group II rats were fed with standard diet and group III rats were fed with standard diet plus ASU pills for 10 days. One day after electrocauterization of bilateral vertebral arteries for groups II and III, bilateral common carotid arteries were occluded for 30 min and then reperfused for 30 min. After these procedures, rats of all groups were sacrificed. The levels of malondialdehyde (MDA) and nitric oxide (NO) and activities of superoxide dismutase (SOD) and catalase (CAT) were measured in the left hippocampus. The number of apoptotic neurons was counted by Tunel method in histological samples of right hippocampus.


RESULTS
MDA and NO levels increased in group II compared with group I rats (p = 0.002, p = 0.015). In group III, MDA and NO levels decreased as compared to group II (p = 0.041, p = 0.002). SOD and CAT activities increased in group III as compared to group II rats (p = 0.002, p = 0.002). The number of apoptotic neurons was lower in group III as compared to group II rats.


CONCLUSIONS
The present findings suggest that ASU could decrease oxidative stress and apoptotic changes in ischemic rat hippocampus. Dietary supplementation of ASU may be beneficial to prevent or ameliorate ischemic cerebral vascular disease.
Yaman
Mehmet
M
Department of Neurology, School of Medicine, Kocatepe University, Afyonkarahisar, Turkey. yaman@aku.edu.tr
Eser
Olcay
O
Cosar
Murat
M
Bas
Orhan
O
Sahin
Onder
O
Mollaoglu
Hakan
H
Fidan
Huseyin
H
Songur
Ahmet
A
D000284:Administration, Oral; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000627:therapeutic use*; D017209:Apoptosis; D002545:Brain Ischemia / Q000097:blood / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D002374:Catalase / Q000097:blood / Q000378:metabolism; D005260:Female; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology; D020287:In Situ Nick-End Labeling; D008315:Malondialdehyde / Q000097:blood / Q000378:metabolism; D009569:Nitric Oxide / Q000097:blood / Q000378:metabolism; D018384:Oxidative Stress; D027421:Persea; D008517:Phytotherapy; D010938:Plant Oils / Q000008:administration & dosage / Q000627:therapeutic use*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000097:blood / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D013025:Glycine max; D013482:Superoxide Dismutase / Q000097:blood / Q000378:metabolism
D000975:Antioxidants; D010938:Plant Oils; D009569:Nitric Oxide; D008315:Malondialdehyde; D002374:Catalase; D013482:Superoxide Dismutase