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The ent-kaurane diterpenoid enriched fraction (EDEF) of maize root was isolated and purified, and 10 compounds, including 4 ent-kaurane diterpenoids, were isolated and identified. We evaluated their neuroprotective properties in vitro for the first time using an H 2 O 2 -induced oxidative damage model in SH-SY5Y cells. The results showed that pretreatment with maizediterpene D, a new ent-kaurane diterpenoid isolated from the EDEF, significantly attenuated H 2 O 2 -induced apoptosis by improving cell survival, reducing ROS production and increasing mitochondrial membrane potential. Mechanistically, the neuroprotective effect of maizediterpene D was confirmed to be related to the dual activation of IGF-1R and BDNF/TrkB crosstalk pathways. Our findings suggest that the EDEF and its active constituent maizediterpene D had good neuroprotective properties and could serve as potential candidates for the development of therapeutic drugs for oxidative stress-related diseases. [Display omitted] • EDEF and Maizediterpene D were isolated from maize roots. • EDEF showed good antioxidant activity against H 2 O 2 induced oxidative stress. • D showed better cytoprotective activity against H 2 O 2 triggered oxidative stress. • M-D attenuated H 2 O 2 induced oxidative stress by BDNF/TrkB and BDNF/TrkB crosstalk pathways [ABSTRACT FROM AUTHOR]

The acquired resistance to gefitinib limits its clinical application. Epigallocatechin-3-gallate (EGCG) has been found to enhance the efficacy of gefitinib against resistant. However, the cellular and molecular mechanisms have not been completely illuminated in NSCLC. In this study, a new epigallocatechin gallate derivative (2R,3R-6-methoxycarbonylgallocatechin-3- O -gallate, the following referred to as EGCGD) (1) and three known epigallocatechin gallate compounds including epicatechin-3- O -gallate (2), gallocatechin-3- O -gallate (3) and epigallocatechin-3- O -gallate (4 , EGCG) were isolated and identified from Anhua dark tea. The pharmacological studies showed EGCGD was more effective against gefitinib-resistant HCC827-Gef cells compared to that of other three epigallocatechin gallate compounds including EGCG, suggesting that introduction of 6-methoxycarbonyl to EGCG might enhance its antitumor activities. Further study on molecular mechanism showed EGCGD increased the potency of gefitinib against HCC827-Gef cells via suppression of epithelial-Mesenchymal transition (EMT) and dual inhibition of PI3K/mTOR. Unlabelled Image [ABSTRACT FROM AUTHOR]