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Choi JH, Jang M, Kim EJ, et al. Oriental Medicine Woohwangchungsimwon Attenuates Kainic Acid-Induced Seizures and Neuronal Cell Death in the Hippocampus. Rejuvenation Res. 2016;19(5):394-405doi: 10.1089/rej.2015.1779.
Choi, J. H., Jang, M., Kim, E. J., Kim, H., Ye, S. K., & Cho, I. H. (2016). Oriental Medicine Woohwangchungsimwon Attenuates Kainic Acid-Induced Seizures and Neuronal Cell Death in the Hippocampus. Rejuvenation research, 19(5), 394-405. https://doi.org/10.1089/rej.2015.1779
Choi, Jong Hee, et al. "Oriental Medicine Woohwangchungsimwon Attenuates Kainic Acid-Induced Seizures and Neuronal Cell Death in the Hippocampus." Rejuvenation research vol. 19,5 (2016): 394-405. doi: https://doi.org/10.1089/rej.2015.1779
Choi JH, Jang M, Kim EJ, Kim H, Ye SK, Cho IH. Oriental Medicine Woohwangchungsimwon Attenuates Kainic Acid-Induced Seizures and Neuronal Cell Death in the Hippocampus. Rejuvenation Res. 2016 Oct;19(5):394-405. doi: 10.1089/rej.2015.1779. Epub 2016 Mar 16. PMID: 26981959.
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Rejuvenation Res. 2016 Oct;19(5):394-405. doi: 10.1089/rej.2015.1779. Epub 2016 Mar 16.

Oriental Medicine Woohwangchungsimwon Attenuates Kainic Acid-Induced Seizures and Neuronal Cell Death in the Hippocampus.

Rejuvenation research

Jong Hee Choi, Minhee Jang, Eun-Jeong Kim, Hocheol Kim, Sang-Kyu Ye, Ik-Hyun Cho

Affiliations

  1. 1 Department of Convergence Medical Science, College of Korean Medicine, Kyung Hee University , Seoul, Republic of Korea.
  2. 2 Brain Korea 21 Plus Program, College of Korean Medicine, Kyung Hee University , Seoul, Republic of Korea.
  3. 3 Department of Herbology, College of Korean Medicine, Kyung Hee University , Seoul, Republic of Korea.
  4. 4 Institute of Korean Medicine, College of Korean Medicine, Kyung Hee University , Seoul, Republic of Korea.
  5. 5 Department of Pharmacology, Seoul National University College of Medicine , Seoul, Republic of Korea.

PMID: 26981959 DOI: 10.1089/rej.2015.1779

Abstract

Woohwangchungsimwon (WCW) is an oriental medicine that has been extensively prescribed in Asia to patients with apoplexy, high blood pressure, acute/chronic convulsion, and so on. However, the potential therapeutic value of WCW in treating the pathologic brain has not yet been fully investigated. In the present study, we evaluated whether WCW has beneficial effects on kainic acid (KA)-induced excitotoxicity. An intraperitoneal injection of KA (40 mg/kg) and an intracerebroventricular injection of KA (0.2 μg) produced typical seizure behavior and neuronal cell death in the CA1 and CA3 pyramidal layers of the hippocampus, respectively. However, the systemic administration of WCW significantly attenuated the seizure behavior and neuronal cell death. WCW was found to exert the best protective effect when it was administrated 2 hours before a KA injection. Moreover, this WCW-induced neuroprotection was accompanied by a reduction in microglia activation and tumor necrosis factor-alpha, interleukin (IL)-1β, IL-6, inducible nitric oxide synthase, and cyclooxyganase-2 in the hippocampus. These results suggest that WCW has therapeutic potential to suppress KA-induced pathogenesis in the brain by inhibiting inflammation.

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