1. Asiatic acid and maslinic acid attenuated kainic acid-induced seizure through decreasing hippocampal inflammatory and oxidative stress.
- Author
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Wang ZH, Mong MC, Yang YC, and Yin MC
- Subjects
- Animals, Anti-Inflammatory Agents, Non-Steroidal chemistry, Anti-Inflammatory Agents, Non-Steroidal pharmacology, Anticonvulsants chemistry, Antioxidants chemistry, Antioxidants pharmacology, Apoptosis drug effects, Apoptosis physiology, Dose-Response Relationship, Drug, Hippocampus immunology, Kainic Acid, Male, Mice, Inbred C57BL, Oxidative Stress physiology, PC12 Cells, Pentacyclic Triterpenes chemistry, Rats, Seizures metabolism, Triterpenes chemistry, Anticonvulsants pharmacology, Hippocampus drug effects, Oxidative Stress drug effects, Pentacyclic Triterpenes pharmacology, Seizures drug therapy, Triterpenes pharmacology
- Abstract
Seizure is a neurological disorder including hippocampal oxidative and inflammatory stress, and glutamate toxicity. Thus, any agent(s) that mitigate(s) these events in hippocampus might attenuate seizure severity. The effects of asiatic acid (AA) or maslinic acid (MA) pre-administration at 20 or 40mg/kg body weight/day upon inflammatory, oxidative and apoptotic injury in hippocampus of kainic acid (KA)-treated mice were examined. KA induced seizure-like behavioral patterns, which was attenuated by AA or MA pre-administration. KA stimulated the release of interleukin (IL)-1beta, IL-6, tumor necrosis factor-alpha and prostaglandin E
2 in hippocampus of mice. AA or MA pre-administration decreased the production of these inflammatory factors. AA or MA also diminished KA-induced increase in hippocampal cyclooxygenase-2 activity and relative NF-κB p50/65 binding activity. KA depleted glutathione content and promoted reactive oxygen species generation. AA or MA pre-administration reversed these alterations. KA lowered Bcl-2 mRNA expression and increased Bax mRNA expression. AA or MA treatments reduced Bax mRNA expression. AA or MA pre-administration enhanced glutamine synthetase activity, decreased glutamate level and increased glutamine level in hippocampus of KA treated mice. In addition, AA or MA pre-treatments at 10 and 20μM increased viability and decreased plasma membrane damage in KA treated nerve growth factor (NGF)-differentiated PC12 cells. Both agents also lowered the release of calcium ion induced by KA in NGF-treated PC12 cells. These findings support that asiatic acid and maslinic acid are potent nutraceutical agents for seizure alleviation., (Copyright © 2017 Elsevier B.V. All rights reserved.)- Published
- 2018
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