Antiepileptic Effect of Uncaria rhynchophylla and Rhynchophylline Involved in the Initiation of c-Jun N-Terminal Kinase Phosphorylation of MAPK Signal Pathways in Acute Seizures of Kainic Acid-Treated Rats

Article English OPEN
Hsin-Cheng Hsu ; Nou-Ying Tang ; Chung-Hsiang Liu ; Ching-Liang Hsieh (2013)
  • Publisher: Hindawi Limited
  • Journal: Evidence-Based Complementary and Alternative Medicine, volume 2,013 (issn: 1741-427X, eissn: 1741-4288)
  • Related identifiers: doi: 10.1155/2013/961289, pmc: PMC3867957
  • Subject: Other systems of medicine | Research Article | RZ201-999 | Article Subject

Seizures cause inflammation of the central nervous system. The extent of the inflammation is related to the severity and recurrence of the seizures. Cell surface receptors are stimulated by stimulators such as kainic acid (KA), which causes intracellular mitogen-activated protein kinase (MAPK) signal pathway transmission to coordinate a response. It is known that Uncaria rhynchophylla (UR) and rhynchophylline (RP) have anticonvulsive effects, although the mechanisms remain unclear. Therefore, the purpose of this study is to develop a novel strategy for treating epilepsy by investigating how UR and RP initiate their anticonvulsive mechanisms. Sprague-Dawley rats were administered KA (12 mg/kg, i.p.) to induce seizure before being sacrificed. The brain was removed 3 h after KA administration. The results indicate that pretreatment with UR (1.0 g/kg), RP (0.25 mg/kg), and valproic acid (VA, 250 mg/kg) for 3 d could reduce epileptic seizures and could also reduce the expression of c-Jun aminoterminal kinase phosphorylation (JNKp) of MAPK signal pathways in the cerebral cortex and hippocampus brain tissues. Proinflammatory cytokines interleukin (IL)-1β, IL-6, and tumor necrosis factor-α remain unchanged, indicating that the anticonvulsive effect of UR and RP is initially involved in the JNKp MAPK signal pathway during the KA-induced acute seizure period.
  • References (32)
    32 references, page 1 of 4

    Schultzberg, M., Lindberg, C., Aronsson, Å. F., Hjorth, E., Spulber, S. D., Oprica, M.. Inflammation in the nervous system: physiological and pathophysiological aspects. Physiology and Behavior. 2007; 92 (1-2): 121-128

    Vezzani, A., French, J., Bartfai, T., Baram, T. Z.. The role of inflammation in epilepsy. Nature Reviews Neurology. 2011; 7 (1): 31-40

    Li, G., Bauer, S., Nowak, M., Norwood, B., Tackenberg, B., Rosenow, F., Knake, S., Oertel, W. H., Hamer, H. M.. Cytokines and epilepsy. Seizure. 2011; 20 (3): 249-256

    Mattson, M. P., Camandola, S.. NF-κB in neuronal plasticity and neurodegenerative disorders. The Journal of Clinical Investigation. 2001; 107 (3): 247-254

    Lerner-Natoli, M., Montpied, P., Rousset, M., Bockaert, J., Rondouin, G.. Sequential expression of surface antigens and transcription factor NFκB by hippocampal cells in excitotoxicity and experimental epilepsy. Epilepsy Research. 2000; 41 (2): 141-154

    Lubin, F. D., Ren, Y., Xu, X., Anderson, A. E.. Nuclear factor-κB regulates seizure threshold and gene transcription following convulsant stimulation. Journal of Neurochemistry. 2007; 103 (4): 1381-1395

    Robinson, M. J., Cobb, M. H.. Mitogen-activated protein kinase pathways. Current Opinion in Cell Biology. 1997; 9 (2): 180-186

    Novelli, A., Tasker, R. A. R.. Excitatory amino acids in epilepsy: from the clinics to the laboratory. Amino Acids. 2007; 32 (3): 295-297

    Li, S.. Bencoogongmu. 2005

    Hsieh, C., Chen, M., Li, T., Li, S., Tang, N., Hsieh, C., Pon, C., Lin, J.. Anticonvulsant effect of Uncaria rhynchophylla (miq) Jack, in rats with kainic acid-induced epileptic seizure. American Journal of Chinese Medicine. 1999; 27 (2): 257-264

  • Similar Research Results (1)
  • Metrics
    No metrics available
Share - Bookmark