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ORIGINAL ARTICLE
Year : 2018  |  Volume : 11  |  Issue : 7  |  Page : 415-422

Attenuation of oxidative stress-induced neuronal cell death by Hydnophytum formicarum Jack.


1 Department of Clinical Microbiology and Applied Technology, Faculty of Medical Technology, Mahidol University, Bangkok 10700, Thailand; Departmcnt of Medical Laboratory Technology, University of Medical Technology, Yangon 11012, Myanmar
2 Department of Clinical Microbiology and Applied Technology; Center for Research and Innovation, Faculty of Medical Technology, Mahidol University, Bangkok 10700, Thailand
3 Center for Research and Innovation, Faculty of Medical Technology, Mahidol University, Bangkok 10700, Thailand
4 Department of Clinical Microbiology and Applied Technology, Faculty of Medical Technology, Mahidol University, Bangkok 10700, Thailand
5 Center of Data Mining and Biomedical Informatics, Faculty of Medical Technology, Mahidol University, Bangkok 10700, Thailand

Correspondence Address:
Kamonrat Phopin
Department of Clinical Microbiology and Applied Technology, Faculty of Medical Technology, Mahidol University, Bangkok 10700
Thailand
Supaluk Prachayasittikul
Center of Data Mining and Biomedical Informatics, Faculty of Medical Technology, Mahidol University, Bangkok 10700
Thailand
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1995-7645.237185

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Objective: To investigate protective effects of Hydnophytum formicarum Jack. (H. formicarum) extracts via regulation of SIRT1-FOXO3a-ADAM10 signaling and antioxidant activity against H2O2-induced neurotoxicity in neuroblastoma SH-SY5Y cells. Methods: Cell viability and apoptosis of neuronal cells pretreated with H. formicarum Jack. extracts under oxidative stress were determined by MTT assay and flow cytometry. The intracellular reactive oxygen species (ROS) was performed using Carboxy-DCFDA assay. Additionally, a profile of protein expressions related to neuroprotection was detected by western blot analysis. Results: The plant extracts (methanol and ethyl acetate) elicited protective effects on the neuronal cell death as performed by the MTT assay and by apoptosis analysis via the activation of BCL-2. Both ethyl acetate and methanol extracts exerted inhibitory effects against H2O2-induced ROS generation in the SH-SY5Y cells. Furthermore, the possible mechanism of neuroprotection of H. formicarum Jack. was observed through its antioxidant properties by maintaining the levels of catalase and SOD2 proteins as well as activating SIRT1-FOXO3a pathway. Importantly, pretreatment of neuronal cells with H. formicarum Jack. significantly recovered the levels of ADAM10 protein compared with the H2O2 treatment alone. Conclusions: The recent findings suggest the protective effects of H. formicarum Jack. plant extracts on attenuating H2O2-induced neurotoxicity in human SH-SY5Y cells.


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