Therapeutic potency of bee pollen against biochemical autistic features induced through acute and sub-acute neurotoxicity of orally administered propionic acid.
BACKGROUND
It is now well documented that postnatal exposure to certain chemicals has been reported to increase the risk of autism spectrum disorder. Propionic acid (PA), as a metabolic product of gut microbiotaandas a commonly used food additive, has been reported to mediate the effects of autism. Results from animal studies may help to identify environmental neurotoxic agents and drugs that can ameliorate neurotoxicity and may thereby aid in the treatment of autism. The present study investigated the ameliorative effects of natural bee pollen against acute and sub-acute brain intoxication induced by (PA) in rats.


METHODS
Twenty-four young male Western Albino ratswere enrolled in the present study. They were classified into four equal groups, eachwith6 rats. The control group received only phosphate buffered saline; the oral buffered PA-treated groups (II and III) received a neurotoxic dose of 750 mg/kg body weight divided in 3 dose of 250 mg/kg body weight/day serving asthe acute group and 750 mg/kg body weight divided in 10 equal dose of 75 mg/kg body weight/day as the sub-acute group. The fourth group received 50 mg bee pollen for 30 days after PA-acute intoxication.


RESULTS
The obtained data showed that the PA-treated groups demonstrated multiple signs of brain toxicity, as indicated by a depletion of serotonin (5HT), dopamine and nor-adrenaline, together withan increase in IFN-γ and caspase 3. Bee pollen was effective in ameliorating the neurotoxic effect of PA. All measured parameters demonstrated minimal alteration in comparison with thecontrol animal than did those of acute and sub-acute PA-treated animals.


CONCLUSIONS
In conclusion, bee pollen demonstrates anti-inflammatory and anti-apoptotic effects while ameliorating the impaired neurochemistry of PA-intoxicated rats.
Department of Pharmaceutical Chemistry, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.
Huda S
HS
Al-Salem
Biochemistry Department, Science College, King Saud University, P.O. Box 22452, 11495, Riyadh, Saudi Arabia.
Ramesa Shafi
RS
Bhat
Autism Research and Treatment Center, Riyadh, Saudi Arabia.|Shaik AL-Amodi Autism Research Chair, King Saud University, Riyadh, Saudi Arabia.|Department of Physiology, Faculty of Medicine, King Saud University, Riyadh, Saudi Arabia.
Laila
L
Al-Ayadhi
Biochemistry Department, Science College, King Saud University, P.O. Box 22452, 11495, Riyadh, Saudi Arabia. elansary@ksu.edu.sa.|Autism Research and Treatment Center, Riyadh, Saudi Arabia. elansary@ksu.edu.sa.|Shaik AL-Amodi Autism Research Chair, King Saud University, Riyadh, Saudi Arabia. elansary@ksu.edu.sa.|Medicinal Chemistry Department, National Research Centre, Dokki, Cairo, Egypt. elansary@ksu.edu.sa.
Afaf
A
El-Ansary
D000818:Animals; D001321:Autistic Disorder / Q000139:chemically induced / Q000188:drug therapy*; D001516:Bees; D001921:Brain / Q000187:drug effects; D004195:Disease Models, Animal; D008297:Male; D011058:Pollen; D011422:Propionates / Q000633:toxicity; D051381:Rats
D011422:Propionates; C029658:propionic acid
Autism; Bee pollen; Caspase 3; Interferon gamma; Neurotransmitters; Propionic acid