Protective role of Panax ginseng extract standardized with ginsenoside Rg3 against acrylamide-induced neurotoxicity in rats.
Acrylamide (ACR) is an industrial neurotoxic chemical that has been recently found in carbohydrate-rich foods cooked at high temperatures. ACR was designated as a probable human carcinogen by IARC (1994) and USEPA (1988). Panax ginseng extract has efficacies such as anticancer, antihypertension, antidiabetes and antinociception. The objective of the current study is to evaluate the protective effects of Panax ginseng extract against ACR-induced toxicity in rats. Sixty adult Sprague Dawley female rats were divided into six groups included a control group, a group treated orally with ACR (50 mg kg(-1) body weight; b.w.) for 11 days, a group treated orally with Panax ginseng extract (20 mg kg(-1) b.w.) for 11 days and groups treated orally with Panax ginseng for 11 days before, during or after 11 days of ACR treatment. The results indicated that treatment with ACR alone resulted in a significant increase in lipid peroxidation level and LDH activity in brain homogenate as well as in serum CK activity, whereas it caused a significant decrease in SOD activity and a small but statistically insignificant decrease in Na(+)K(+)-ATPase activity in brain homogenate. Serum serotonin, corticosterone, T3, T4, TSH, estradiol, progesterone and plasma adrenaline were significantly decreased in ACR-treated rats. Treatment with Panax ginseng before, during or after ACR treatment reduced or partially antagonized the effects induced by ACR towards the normal values of controls. It could be concluded that Panax ginseng extract exhibited a protective action against ACR toxicity and it is worth noting that treatment with Panax ginseng extract before or at the same time as ACR treatment was more effective than when administered after ACR treatment.
Mannaa
Fathia
F
Medical Physiology Department, National Research Centre, Dokki, Cairo, Egypt.
Abdel-Wahhab
Mosaad A
MA
Ahmed
Hanaa H
HH
Park
Myung H
MH
D020106:Acrylamide / Q000633:toxicity*; D000284:Administration, Oral; D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D004334:Drug Administration Schedule; D005260:Female; D015227:Lipid Peroxidation / Q000187:drug effects; D018696:Neuroprotective Agents / Q000302:isolation & purification / Q000592:standards / Q000627:therapeutic use; D020258:Neurotoxicity Syndromes / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D005894:Panax / Q000737:chemistry*; D010936:Plant Extracts / Q000302:isolation & purification / Q000592:standards / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley
D018696:Neuroprotective Agents; D010936:Plant Extracts; D020106:Acrylamide