Antioxidant Activity of Makham Pom (Phyllanthus emblica L.) Fruit and Its Neuroprotective Effect on Hydrogen Peroxide and Glutamate-Induced Neurotoxicity in Mouse Neuroblastoma Cells

Main Article Content

Sadudee Rattanajarasroj

Abstract

Introduction and objective: Oxidative stress has been implicated in pathogenesis of neurodegenerative diseases. Phyllanthus emblica L. (Makham Pom in Thai) fruit has potent antioxidant activity and may be used to alleviate oxidative stress-induced neurodegenerative process. This study was designed to investigate the antioxidative and neuroprotective activities of P. emblica fruits on hydrogen peroxide (H2O2) and glutamate-induced neurotoxicity in N1E-115, mouse neuroblastoma cell cultures.


Methods: P. emblica fruit juice (PE-J), water extract (PE-W) and ethanol extract (PE-E) were used in this study. All samples were evaluated for antioxidative activity using hydroxyl and superoxide scavenging assay. The neuroprotective activity was investigated using hydrogen peroxide (H2O2) and glutamate-induced neurotoxicity in N1E-115 cells. Cell viability was evaluated using 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) reduction assay. Moreover, we also determined the protective effect of P. emblica fruits mediated via mitogen activated protein kinase (MAPK) or phosphatidylinositol 3-kinase (PI3K) sinaling pathway. Inhibitors of intracellular signaling cascade were used in this study.


Results: PE-J, PE-W and PE-E exhibited efficient antioxidant activities. Pre-exposure of cultured neurons with PE-W or PE-E before H2O2 exposure could protect cell injury from H2O2 while co-exposure of cultured neurons to H2O2 with each sample did not show this beneficial effect. Both pre-exposure and co-exposure with all samples did not prevent glutamate-induced neurotoxicity in cultured neurons. In addition, PI3K inhibitor prevented PE-W and PE-E-induced neuroprotection, but MAPK inhibitor failed to counteract their protective effects.


Discussion: P. emblica fruits exhibited efficient antioxidant activities which are consistent with previous studies. Pre-exposure of cultured neurons with PE-W or PE-E before H2O2 exposure could protect cell injury from H2O2. It is possible that the protective effect might at least partly result from their antioxidative properties. PI3K inhibitor prevented PE-W and PE-E-induced neuroprotection against H2O2, suggesting that the neuroprotective mechanisms might involve PI3K signaling pathway.


Conclusion and recommendation:  This study indicated that P. emblica fruits showed the neuroprotective effect on H2O2-induced neurotoxicity. The neuroprotective mechanisms might partly involve an antioxidant property and PI3K signaling pathway. It is suggested that further studies on other degenerative models and animal models are required to clarify its efficacy and delineate the underlying mechanisms prior to the development as herbal health products.

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References

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