2013
DOI: 10.1155/2013/961289
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Antiepileptic Effect ofUncaria rhynchophyllaandRhynchophyllineInvolved in the Initiation of c-Jun N-Terminal Kinase Phosphorylation of MAPK Signal Pathways in Acute Seizures of Kainic Acid-Treated Rats

Abstract: 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 th… Show more

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Cited by 25 publications
(15 citation statements)
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“…In a rat model of ischemia, valproic acid at a human equivalent dose of 2919 mg was found to reduce myeloperoxidase and ionized calcium binding adapter molecule 1 staining (Suda et al 2013), the possibility that the failure of valproic acid to reduce the expression of the pro-inflammatory markers observed here in the hippocampus was related to the use of a low dose cannot be completely discarded. However, valproic acid administered to rats at a high human equivalent dose (2432 mg) for 3 days also failed to modify the expression of IL-1b and TNF-a in the hippocampus (Hsu et al 2013).…”
Section: Discussionmentioning
confidence: 92%
See 1 more Smart Citation
“…In a rat model of ischemia, valproic acid at a human equivalent dose of 2919 mg was found to reduce myeloperoxidase and ionized calcium binding adapter molecule 1 staining (Suda et al 2013), the possibility that the failure of valproic acid to reduce the expression of the pro-inflammatory markers observed here in the hippocampus was related to the use of a low dose cannot be completely discarded. However, valproic acid administered to rats at a high human equivalent dose (2432 mg) for 3 days also failed to modify the expression of IL-1b and TNF-a in the hippocampus (Hsu et al 2013).…”
Section: Discussionmentioning
confidence: 92%
“…However, valproic acid administered to rats at a high human equivalent dose (2432 mg) for 3 days also failed to modify the expression of IL‐1β and TNF‐α in the hippocampus (Hsu et al . ).…”
Section: Discussionmentioning
confidence: 97%
“…IL-1β through binding to IL-1R1 and TNFα activate transcription factors such as NF-κB which regulates the synthesis of chemokines, cytokines, enzymes (for example, CoX-2) and receptors (for example, TLRS, IL-1R1, and TNF p55 and p75 receptors) that are involved in epileptogenesis [29] . NF-κB activation can also induce the generation of neurotoxic free radicals; resulting in neuronal apoptosis [30] . In addition, occupancy of IL-1R1 or TLRS results in activation of src tyrosine kinase, mitogen activated protein kinases (MAPK) system with subsequent induction of neuronal cyclic adenosine monophosphate (cAMP) response element-binding protein [31] .…”
Section: Zaki Y ; Et Al…… -596-discussionmentioning
confidence: 99%
“…In vitro, 5 μg/μL of rhynchophylline can inhibit the production of IL-1β and TNF-α in dopaminergic neurons and glial cells induced by lipopolysaccharide, so as to protect neurons. Rhynchophylline can also inhibit the phosphorylation of p38 MAPK, then block the nuclear translocation of NF-κB, and inhibit its transcriptional function, so as to inhibit the vascular endothelial cell damage caused by intermittent hypoxia [87].…”
Section: Indole Alkaloidmentioning
confidence: 99%