Expression pattern of NMDA receptors reveals antiepileptic potential of apigenin 8-C-glucoside and chlorogenic acid in pilocarpine induced epileptic mice |
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| Institution: | 1. Department of Environmental Biotechnology, Bharathidasan University, Tiruchirappalli 620 024, Tamilnadu, India;2. Central Inter-Disciplinary Research Facility, Mahatma Gandhi Medical College and Research Institute Campus, Pillayarkuppam, Puducherry 607 402, India;3. Department of Biotechnology, Anna University, Tiruchirappalli 620 024, Tamilnadu, India;1. Guangxi Medical University, Nanning 530021, China;2. The First Affiliated Hospital of Guangxi University of Chinese Medicine, Nanning 530023, China;3. Department of Biochemistry, University of Arkansas Medical School, 4301 W. Markham, Little Rock, AR 72205-7199, USA;1. College of Food Engineering and Nutritional Science, Shaanxi Normal University, Xi’an 710119, China;2. Laboratory of Functional Chemistry and Nutrition of Food, College of Food Science and Engineering, Northwest A&F University, Yangling 712100, China;1. Department of Neurology, Linzi Maternal & Child Health Hospital of Zibo, Zibo, Shandong, China;2. Department of Applied Biology and Chemical Technology, The Hong Kong Polytechnic University, Hong Kong, China;3. Shenzhen Research Institute of the Hong Kong Polytechnic University, State Key Laboratory of Chinese Medicine and Molecular Pharmacology (Incubation), Shenzhen, Guangdong, China;4. Department of Pathophysiology, Medical College, Qingdao University, Qingdao, Shandong, China;5. Department of Biomedical Sciences, City University of Hong Kong, Hong Kong, China;1. Key Laboratory of Tibetan Medicine Research, Northwest Institute of Plateau Biology, Chinese Academy of Sciences, Xining 810008, PR China;2. Key Laboratory of Chemistry of Northwestern Plant Resources of CAS and Key Laboratory for Natural Medicine of Gansu Province, Lanzhou Institute of Chemical Physics, Chinese Academy of Sciences, Lanzhou 730000, PR China;3. State Key Laboratory of Phytochemistry and Plant Resources in West China, Kunming Institute of Botany, Chinese Academy of Sciences, Kunming 650204, PR China;1. Department of Physiology, University of Auckland, Auckland, New Zealand;2. Department of Chemistry, Department of Molecular Biosciences, Chemistry of Life Processes Institute, Center for Molecular Innovation and Drug Discovery, Northwestern University, Evanston, IL 60208-3113, USA;3. Department of Pediatrics, NorthShore University HealthSystem, Evanston, IL, USA;4. Department of Chemistry, University of Utah, Salt Lake City, UT, USA;1. Department of Neurology, Guangzhou Hospital of Traditional Chinese Medicine, Guangzhou, Guangdong, 510130, China;2. College of Allied Health Professions, Shanghai University of Medicine and Health Sciences, Shanghai, 201318, China;3. Department of Clinical Laboratory Medicine, Guangdong General Hospital, Guangzhou, Guangdong, 510030, China;4. Gynecology Department, Shanghai Traditional Chinese Medicine Hospital, Shanghai, 200071, China |
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| Abstract: | The present study was aimed to evaluate the effect of apigenin 8-C-glucoside (Vitexin) and chlorogenic acid on epileptic mice induced by pilocarpine and explored its possible mechanisms. Intraperitonial administration of pilocarpine (85 mg/kg) induced seizure in mice was assessed by behavior observations, which is significantly (p > 0.05) reduced by apigenin 8-C-glucoside (AP8CG) (10 mg/kg) and chlorogenic acid (CA) (5 mg/kg), similar to diazepam. Seizure was accompanied by an imbalance in the levels of Gamma-aminobutyric acid (GABA) and glutamate in the pilocarpine administered group. Moreover, convulsion along with reduced acetylcholinesterase, increased monoamine oxidase and oxidative stress was observed in epileptic mice brain. AP8CG and CA significantly restored back to normal levels even at lower doses. Further, increased lipid peroxidation and nitrite content was also significantly attenuated by AP8CG and CA. However, CA was found to be more effective when compared to AP8CG. In addition, the mRNA expression of N-methyl-d-aspartate receptor (NMDAR), mGluR1 and mGlu5 was significantly (P ≤ 0.05) inhibited by AP8CG and CA in a lower dose. The mRNA expression of GRIK1 did not differ significantly in any of the group and showed a similar pattern of expression. Our result shows that AP8CG and CA selectively inhibit NMDAR, mGluR1 and mGlu5 expression. Modification in the provoked NMDAR calcium response coupled with neuronal death. Hence, these findings underline that the polyphenolics, AP8CG and CA have exerted antiepileptic and neuroprotective activity by suppressing glutamate receptors. |
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| Keywords: | Epilepsy Acetylcholinesterase NMDAR Antioxidant Apigenin 8-C-glucoside Chlorogenic acid |
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