<i>Cissus verticillata</i> Extract Decreases Neuronal Damage Induced by Oxidative Stress in HT22 Cells and Ischemia in Gerbils by Reducing the Inflammation and Phosphorylation of MAPKs
Woosuk Kim,
Hyun Jung Kwon,
Hyo Young Jung,
Soon-Sung Lim,
Beom-Goo Kang,
Yong-Bok Jo,
Dong-Sool Yu,
Soo Young Choi,
In Koo Hwang,
Dae Won Kim
Affiliations
Woosuk Kim
Department of Biomedical Sciences, and Research Institute for Bioscience and Biotechnology, Hallym University, Chuncheon 24252, Korea
Hyun Jung Kwon
Department of Biomedical Sciences, and Research Institute for Bioscience and Biotechnology, Hallym University, Chuncheon 24252, Korea
Hyo Young Jung
Department of Veterinary Medicine, Institute of Veterinary Science, Chungnam National University, Daejeon 34134, Korea
Soon-Sung Lim
Department of Food Science and Nutrition, Institute of Korean Nutrition, Hallym University, Chuncheon 24252, Korea
Beom-Goo Kang
Department of Biochemistry, College of Medicine, Hallym University, Chuncheon 24252, Korea
Yong-Bok Jo
Department of Convergence Technology, Graduate School of Venture, Hoseo University, Seoul 06724, Korea
Dong-Sool Yu
Department of Venture Management Graduate School of Venture, Hoseo University, Seoul 06724, Korea
Soo Young Choi
Department of Biomedical Sciences, and Research Institute for Bioscience and Biotechnology, Hallym University, Chuncheon 24252, Korea
In Koo Hwang
Department of Anatomy and Cell Biology, College of Veterinary Medicine and Research Institute for Veterinary Science, Seoul National University, Seoul 08826, Korea
Dae Won Kim
Department of Biochemistry and Molecular Biology, Research Institute of Oral Sciences, College of Dentistry, Gangneung-Wonju National University, Gangneung 25457, Korea
In the present study, we examined the effects of Cissus verticillata leaf extracts (CVE) against hydrogen peroxide (H2O2)- and ischemia-induced neuronal damage in HT22 cells and gerbil hippocampus. Incubation with CVE produced concentration-dependent toxicity in HT22 cells. Significant cellular toxicity was observed with >75 μg/mL CVE. CVE treatment at 50 μg/mL ameliorated H2O2-induced reactive oxygen species formation, DNA fragmentation, and cell death in HT22 cells. In addition, incubation with CVE significantly mitigated the increase in Bax and decrease in Bcl-2 induced by H2O2 treatment in HT22 cells. In an in vivo study, the administration of CVE to gerbils significantly decreased ischemia-induced motor activity 1 d after ischemia, as well as neuronal death and microglial activation 4 d after ischemia, respectively. CVE treatment reduced the release of interleukin-1β, interleukin-6, and tumor necrosis factor-α 6 h after ischemia. Furthermore, CVE treatment significantly ameliorated ischemia-induced phosphorylation of c-Jun N-terminal kinase, extracellular signal-regulated kinase 1/2, and p38. These results suggest that CVE has the potential to reduce the neuronal damage induced by oxidative and ischemic stress by reducing the inflammatory responses and phosphorylation of MAPKs, suggesting that CVE could be a functional food to prevent neuronal damage induced by ischemia.
