Key result
Epigallocatechin gallate (EGCG) dose-dependently improved the anti-angiogenic state, promoted cell viability, and suppressed hypoxia-induced endothelial dysfunction in trophoblast cells by downregulating HMGB1.
Why the study?
Preeclampsia is a serious pregnancy complication lacking effective therapy, prompting investigation into whether epigallocatechin gallate (EGCG) could reduce anti-angiogenic factors, improve cell viability, and suppress endothelial dysfunction via HMGB1 regulation.
Does EGCG improve anti-angiogenic state, cell viability, and hypoxia-induced endothelial dysfunction in an in vitro model of preeclampsia?
Does EGCG improve anti-angiogenic state, cell viability, and hypoxia-induced endothelial dysfunction in an in vitro model of preeclampsia?
EGCG improves endothelial dysfunction and cell viability in an in vitro preeclampsia model by downregulating HMGB1, suggesting potential as a novel therapeutic candidate.
BACKGROUND Preeclampsia (PE) is a serious complication of pregnancy with no effective therapy. This study assessed whether epigallocatechin gallate (EGCG) could reduce the production of anti-angiogenic factors, improve cell viability, and suppress endothelial dysfunction in vitro via regulating high mobility group box 1 (HMGB1) in preeclampsia. MATERIAL AND METHODS Human umbilical vein endothelial cells (HUVECs) grown in conditioned medium from hypoxic JEG-3 cells were used to investigate the effects of EGCG on anti-angiogenic state, cell viability, and markers of endothelial dysfunction. To confirm that EGCG exerted its effects via HMGB1, we also examined the impact of EGCG on anti-angiogenic state, cell viability, and endothelial dysfunction following HMGB1 treatment in vitro. RESULTS EGCG inhibited HMGB1 expression in hypoxic trophoblast cells in a dose-dependent manner. In addition, EGCG relieved anti-angiogenic state and endothelial dysfunction in hypoxic trophoblast cells by downregulating HMGB1. Moreover, EGCG dose-dependently promoted cell proliferation by downregulating HMGB1. CONCLUSIONS Taken together, our data show the protective role of EGCG in preeclampsia and revealed EGCG-mediated effects on the production of anti-angiogenic factors, cell viability, and endothelial dysfunction through downregulating HMGB1. These observations suggest that EGCG is a novel therapeutic candidate for preeclampsia.
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Zhong et al. (2020) studied Preeclampsia (in vitro model). Epigallocatechin Gallate (EGCG) vs. Hypoxic conditions without EGCG was evaluated on HMGB1 expression, anti-angiogenic state, cell viability, and endothelial dysfunction. Epigallocatechin gallate (EGCG) dose-dependently improved the anti-angiogenic state, promoted cell viability, and suppressed hypoxia-induced endothelial dysfunction in trophoblast cells by downregulating HMGB1.
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