Increased cyclooxygenase-2 and nuclear factor-κB/p65 expression in mouse hippocampi after systemic administration of tetanus toxin.
Brain inflammation has a crucial role in various diseases of the central nervous system. The hippocampus in the mammalian brain exerts an important memory function, which is sensitive to various insults, including inflammation induced by exo/endotoxin stimuli. Tetanus toxin (TeT) is an exotoxin with the capacity for neuronal binding and internalization. The present study investigated changes in inflammatory mediators in the mouse hippocampus proper (CA1‑3 regions) and dentate gyrus (DG) after TeT treatment. The experimental mice were intraperitoneally injected with TeT at a low dosage (100 ng/kg), while the control mice were injected with the same volume of saline. At 6, 12 and 24 h after TeT treatment, changes in the hippocampal levels of inflammatory mediators cyclooxygenase‑2 (COX‑2) and nuclear factor kappa‑B (NF‑κB/p65) were assessed using immunohistochemical and western blot analysis. In the control group, moderate COX‑2 immunoreactivity was observed in the stratum pyramidal (SP) of the CA2‑3 region, while almost no expression was identified in the CA1 region and the DG. COX‑2 immunoreactivity was increased by TeT in the SP and granule cell layer (GCL) of the DG in a time‑dependent manner. At 24 h post‑treatment, COX‑2 immunoreactivity in the SP of the CA1 region and in the GCL of the DG was high, and COX‑2 immunoreactivity in the SP of the CA2/3 region was highest. Furthermore, the present study observed that NF‑κB/p65 immunoreactivity was obviously increased in the SP and GCL at 6, 12 and 24 h after TeT treatment. In conclusion, the present study demonstrated that systemic treatment with TeT significantly increased the expression of COX-2 and NF-κB/p65 in the mouse hippocampus, suggesting that increased COX‑2 and NF-κB/65 expression may be associated with inflammation in the brain induced by exotoxins.
Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, Yangzhou, Jiangsu 225001, P.R. China.
Bing Chun
BC
Yan
Department of Radiology, School of Medicine, Kangwon National University, Chuncheon, Gangwon 200‑701, Republic of Korea.
Yong Hwan
YH
Jeon
Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, Gangwon 200‑701, Republic of Korea.
Joon Ha
JH
Park
Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, Gangwon 200‑701, Republic of Korea.
In Hye
IH
Kim
Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, Gangwon 200‑701, Republic of Korea.
Jeong-Hwi
JH
Cho
Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, Gangwon 200‑701, Republic of Korea.
Ji Hyeon
JH
Ahn
Department of Physiology, College of Medicine, Hallym University, Chuncheon, Gangwon 200‑702, Republic of Korea.
Bai Hui
BH
Chen
Department of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon, Gangwon 200‑702, Republic of Korea.
Hyun-Jin
HJ
Tae
Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, Gangwon 200‑701, Republic of Korea.
Jae-Chul
JC
Lee
Department of Emergency Medicine, Sacred Heart Hospital, College of Medicine, Hallym University, Anyang, Gyeonggi 431‑796, Republic of Korea.
Ji Yun
JY
Ahn
Department of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon, Gangwon 200‑701, Republic of Korea.
Dong Won
DW
Kim
Department of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon, Gangwon 200‑701, Republic of Korea.
Jun Hwi
JH
Cho
Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, Gangwon 200‑701, Republic of Korea.
Moo-Ho
MH
Won
Department of Surgery, School of Medicine, Kangwon National University, Chuncheon, Gangwon 200‑701, Republic of Korea.
Seongkweon
S
Hong
D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism* / Q000502:physiology; D018891:Dentate Gyrus / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D006624:Hippocampus / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D007249:Inflammation / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism* / Q000502:physiology; D013744:Tetanus Toxin / Q000633:toxicity*; D051996:Transcription Factor RelA / Q000378:metabolism
D016328:NF-kappa B; D013744:Tetanus Toxin; D051996:Transcription Factor RelA; D051546:Cyclooxygenase 2