Green tea ameliorates recognition memory defects in acute radiation syndrome caused by gamma irradiation.
- Author:
Jong Sik JANG
1
;
Changjong MOON
;
Jong Choon KIM
;
Uhee JUNG
;
Sung Kee JO
;
Sung Ho KIM
Author Information
1. College of Animal Science, Kyungpook National University, Sangju 742-711, Korea.
- Publication Type:Original Article
- Keywords:
green tea;
radiation;
memory impairment;
neurogenesis;
apoptosis
- MeSH:
Acute Radiation Syndrome*;
Adult;
Animals;
Apoptosis;
Autopsy;
Body Weight;
Dentate Gyrus;
Humans;
In Situ Nick-End Labeling;
Memory Disorders;
Memory*;
Mice;
Neurogenesis;
Tea*
- From:Journal of Biomedical Research
2014;15(2):62-67
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
An evidence suggests that even low-dose irradiation can lead to progressive cognitive decline as well as memory deficits in both humans and experimental animals in part due to hippocampal dysfunction. To determine whether or not green tea (GT) and epigallocatechin gallate (EGCG) could attenuate memory impairment as well as suppress hippocampal neurogenesis, passive avoidance and object recognition memory test as well as TUNEL assay and immunohistochemical detection with markers of neurogenesis (Ki-67 and doublecortin (DCX)) were performed using adult mice treated with relatively low-dose gamma irradiation (2.0 Gy). GT was administered intraperitonially at a dosage of 50 mg/kg of body weight at 36 and 12 hr preirradiation and at 30 minutes post-irradiation, or orally at a dosage of 250 mg/kg of body weight/day for 7 days before autopsy. EGCG (25 mg/kg of body weight) was administered intraperitonially at 36 and 12 hr pre-irradiation and at 30 minutes post-irradiation. In the passive avoidance and object recognition memory test, mice trained for 1 day after acute irradiation (2 Gy) showed significant memory deficits compared with sham controls. The number of TUNEL-positive apoptotic nuclei in the dentate gyrus increased by 12 h after irradiation. In addition, the numbers of Ki-67- and DCX-positive cells significantly decreased. GT treatment prior to irradiation attenuated memory defects, blocked apoptotic death, as well as reduced the number of DCX-positive cells. Therefore, GT may attenuate memory defects in adult mice exposed to a relatively low dose of radiation possibly by inhibiting the detrimental effects of irradiation on hippocampal neurogenesis.
