RESUMO
Brain cell damage that results from oxidative toxicity contributes to neuronal degeneration. The transcription factor nuclear factorE2related factor 2 (Nrf2) regulates the expression of heme oxygenase (HO)1 and glutathione (GSH), and serves a key role in the pathogenesis of neurological diseases. Brassica rapa is a turnip that is unique to Ganghwa County, and is used mainly for making kimchi, a traditional Korean food. In the current study, brassicaphenanthrene A (BrPA) from B. rapa was demonstrated to exhibit protective effects against neurotoxicity induced by glutamate via Nrf2mediated HO1 expression. Similarly, BrPA increased the expression of cellular glutathione and glutaminecysteine ligase genes. Furthermore, BrPA caused the nuclear translocation of Nrf2 and increased antioxidant response element (ARE) promoter activity. Nrf2 also mediated HO1 induction by BrPA through the PI3K/Akt and JNK regulatory pathways. The results of the present study indicated the neuroprotective effect of BrPA, a natural food component from B. rapa.
Assuntos
Brassica rapa/química , Heme Oxigenase-1/genética , Fator 2 Relacionado a NF-E2/genética , Fenantrenos/farmacologia , Animais , Elementos de Resposta Antioxidante/genética , Regulação da Expressão Gênica/efeitos dos fármacos , Humanos , Camundongos , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Fármacos Neuroprotetores/farmacologia , Fenantrenos/químicaRESUMO
Oxidative stress contributes to neuronal death in the brain, and neuronal death can cause aging or neurodegenerative disease. Heme oxygenase 1 (HO-1) serves a vital role in the regulation of biological reactions, including oxidative stress associated with reactive oxygen species. In the present study, acerogenin C isolated from the Aceraceae plant Acer nikoense, which is used as a Japanese folk medicine for hepatic disorders and eye diseases. However, there have been no studies on the mechanisms underlying the antineurodegenerative biological activities of acerogenin C. In the present study, acerogenin C demonstrated neuroprotective action against glutamateinduced cell death in hippocampal HT22 cells through the upregulation of HO1 expression. These effects were also associated with nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) and the activation of phosphoinositide 3kinase/protein kinase B. Taken together of the efficacy researches, this study determines that the Nrf2/HO1 pathways denotes a biological mark and that acerogenin C might contribute to prevention of neurodegenerative disorders.