Ophagy signaling. (A) The accumulation of glutamate in ronal death in
Ophagy signaling. (A) The accumulation of glutamate in ronal death in HT-22 diagram of the neuroprotective impact and mechanism of TLE against glutamate-induced neurons leads cells by way of cellular antioxidants and mitophagy signaling. (A) The accumulation of neuronal death in HT-22to the rise in intracellular ROS. The high ROS can destruct the YTX-465 supplier mitochondria and stimulate the excessiveglutamate in selective autophagy of broken mitochondria (mitophagy), neurons leads to the rise in intracellular ROS. The higher ROSresulting in neuronal cell death. On the other stimulate the excessive can destruct the mitochondria and hand, (B) TLE can directly neutralize the ROS and upregulate the gene expression of antioxidant enzymes. These two mechanisms comselective autophagy of damaged mitochondria (mitophagy), health. Furthermore, TLE cancell death. However, (B) TLE can pletely Goralatide Epigenetic Reader Domain inhibit ROS activity and rescue the mitochondrial resulting in neuronal reduce the mitophagy activation, causing a reduce in neuronal cell death. straight neutralize the ROS and upregulate the gene expression of antioxidant enzymes. These two mechanisms totally inhibit ROS activity and rescue theSupplementary Supplies: The following are obtainable on the web at www.mdpi.com/xxx/s1, Figure S1: mitochondrial health. Additionally, TLE can reduce the mitophagy activation, causing a reduce in neuronal cell death. Analysis of bioactive compounds in ethanolic Thunbergia laurifolia leaf extract by liquid chromatography-mass spectrometry (LC-MS) method. Author Contributions: W.V. performed the experiments, analyzed the information and was a significant contributor in writing the manuscript. C.S. performed the experiments and analyzed the information in the bioinformatics part. W.V., M.S. and T.T. conceived the research idea. M.S., K.-W.K. and T.T. provided components for the model study. M.S. and T.T. supervised the research and also corrected the manuscript. All authors study and approved the final manuscript.Figure 10. The summarized diagram from the neuroprotective effect and mechanism of TLE against glutamate-induced neu-Antioxidants 2021, 10,23 ofSupplementary Materials: The following are obtainable online at https://www.mdpi.com/article/ ten.3390/antiox10111678/s1, Figure S1: Evaluation of bioactive compounds in ethanolic Thunbergia laurifolia leaf extract by liquid chromatography-mass spectrometry (LC-MS) method. Author Contributions: W.V. performed the experiments, analyzed the data and was a major contributor in writing the manuscript. C.S. performed the experiments and analyzed the data in the bioinformatics component. W.V., M.S. and T.T. conceived the analysis idea. M.S., K.-W.K. and T.T. provided components for the model study. M.S. and T.T. supervised the investigation and also corrected the manuscript. All authors have study and agreed for the published version in the manuscript. Funding: This operate was financially supported by a scholarship from “The 90th Anniversary of Chulalongkorn University Fund (Ratchadaphiseksomphot Endowment Fund)” funding code GCUGR1125631055M for study expenditures and also “Overseas Study Encounter Scholarship for Graduate Students” from Graduate School, Chulalongkorn University for the research pay a visit to in South Korea. Institutional Evaluation Board Statement: Not applicable. Informed Consent Statement: Not applicable. Information Availability Statement: Data is contained inside the report and Supplementary Components. Acknowledgments: The scholarship for W.V. in the Graduate S.
