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From old remedy to modern therapy: Neuroprotective effects of Semecarpus Anacardium on the l-Monosodium Glutamate treated rats and neuronal cells

Fadwa Al Mughairbi1*, Faisal Khan2, Saima Ilyas3, Yasmeen Shad4 and Muhammad Iqbal Choudhary5
  • 1 United Arab Emirates University, United Arab Emirates
  • 2 Panjwani Center for Molecular Medicine and Drug Research, International Center for Chemical and Biological Sciences , University of Karachi, Pakistan
  • 3 Shaheed Zulfiqar Ali Bhutto Institute of Science and Technology, Pakistan
  • 4 Faculty of Science, University of Technology Sydney, Australia
  • 5 International Center for Chemical and Biological Sciences, University of Karachi, Pakistan

Introduction: Memory may severely decrease throughout aging & evolution of some CNS degeneration pathologies as well as a consequence of oxidative stress & chronic stress. The development of drug effective for dementia widely anticipated because of the increase in the elderly population. Dementia has some histological degeneration in the brain including the hippocampus. Glutamate (Glu) is a major excitatory neurotransmitter found with the central nervous system. It plays an important role in normal neurological functioning such as fast response to stimuli, cognition, memory, movement, and sensation. However, in excessive levels, glutamate is excitotoxic and has been shown to cause neurological damage. Semecarpus Anacardium (SA) has been widely used in folk medicine in Brazil, India, and Africa to treat different conditions, including Arteritis and tumors. In Arabic Folk medicine, it was used to improve memory and reduce inflammation, but very few studies had been done to evaluate its neuroprotective effect. The aim of this study is to evaluate the neuroprotective effect of SA on memory and neurons of lMSG treated rats. Method: 24 Wistar male rats with an average weight of 200g were divided into four groups. Group A was injected with saline and group B was injected with l-monosodium glutamate (lMSG) at a dose of 4g/kg on alternate days for 10 consecutive days (5 doses) while group C and D orally administrated with low (12mg/kg) and high concentrations (24g/kg) of SA along with lMSG respectively. Animals were tested for behavioral tasks including, delayed matching to sample, delayed non-matching to sample & spontaneous alteration (T-Maze). Following that, structural characteristics of the hippocampus were studied using hematoxylin and eosin (H&E) staining. The SA extract was further analyzed for its effect on Glu treated neuronal cells PC-12. Cells were treated with SA extract (dose) and cell survival was assessed by MTT assay (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromidefor) and lactate dehydrogenase (LDH assay). The calcium (Ca) overload induced by Glu was also checked by the Fluorometric assay. Result: In treated animals, SA with two different concentrations induced a different effect on memory. The correct response rate of behavioral tasks in low concentration group was significantly (p<0.05) higher than the lMSG treated group. On the other hand, correct response rate of behavioral tasks was significantly (p<0.05) lower than both the control and the lMSG treated groups when a high dose was used. Histological results also revealed that SA extract protected hippocampal neurons from lMSG induced damage. In the in vitro study, the SA protected the PC-12 cells from Glu induced toxicity significantly as seen both in MTT and LDH assays. The intracellular levels of Ca in PC-12 cells was also decreased significantly by SA treatment. Conclusion: Our results suggest that SA (at low conc) has neuroprotective properties and retrieve both Rats from lMSG induced excitotoxicity. In vitro analysis showed SA effecting neuronal cells by decreasing Ca overload. The results of this study highlights the role of Glu neurotoxicity on neuronal damage, memory and dementia. The results also suggest the possible role of Ca overload as a mediator for this neurotoxicity. Hence, our results shed some light on the assumed mechanism of neuroprotection for future in vivo studies. Keywords: Semecarpus Anacardium, l-Monosodium Glutamate, Neurodegenerative Diseases, Cell Culture, Hippocampus, Behavioral Tasks.

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Keywords: Semecarpus anacardium, l-Mononsodium Glutamate, Neurodegenarative disease, Cell Cullture, Hippocampus, Behavioral tasks

Conference: 4th International Conference on Educational Neuroscience, Abu Dhabi, United Arab Emirates, 10 Mar - 11 Mar, 2019.

Presentation Type: Poster Presentation

Topic: Educational Neuroscience

Citation: Al Mughairbi F, Khan F, Ilyas S, Shad Y and Choudhary M (2019). From old remedy to modern therapy: Neuroprotective effects of Semecarpus Anacardium on the l-Monosodium Glutamate treated rats and neuronal cells. Conference Abstract: 4th International Conference on Educational Neuroscience. doi: 10.3389/conf.fnhum.2019.229.00034

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Received: 07 Mar 2019; Published Online: 27 Sep 2019.

* Correspondence: Dr. Fadwa Al Mughairbi, United Arab Emirates University, Al-Ain, United Arab Emirates, f.almughairbi@uaeu.ac.ae