EGCG attenuates the neurotoxicity of methylglyoxal via regulating MAPK and the downstream signaling pathways and inhibiting advanced glycation end products formation.

Methylglyoxal (MGO), a reactive α-oxoaldehyde formed in many foods and beverages during processing and storage, has neurotoxicity. The purpose of this study was to investigate the inhibition mechanism of (-)-epigallocatechin-3-gallate (EGCG) on MGO-induced PC12 cells damage. Cell apoptosis and reactive oxygen species (ROS) level were measured with fluorescent staining methods. Western blotting was used to detect the signal transduction mechanism. The results indicated that EGCG decreased ROS level, inhibited apoptosis and increased the expression of brain-derived neurotrophic factor. Pathways analysis revealed that the neuroprotective mechanism of EGCG might rely on regulating mitogen-activated protein kinase (MAPK) and downstream pathways. Multi-spectroscopy and molecular docking indicated that EGCG inhibited MGO-derived advanced glycation end products (AGEs) formation. Moreover, the neurotoxicity of AGEs could be alleviated by EGCG. These results suggested that EGCG could attenuate MGO-induced nerve damage via regulating MAPK and downstream pathways and inhibiting AGEs formation.

Exploring the Potential Mechanism of Costunolide-Induced MCF-7 Cells Apoptosis by Multi-Spectroscopy, Molecular Docking and Cell Experiments.

Breast cancer is one of the most common cancer with high morbidity and mortality in women. This study aimed to explore the potential mechanism of costunolide inducing MCF-7 cells apoptosis by multi-spectroscopy, molecular docking, and cell experiments. The results manifested that costunolide interacted with calf thymus DNA (ct-DNA) in a spontaneous manner, and the minor groove as the preferential binding mode. Furthermore, costunolide inhibited cell proliferation and colony formation. Hoechst 33258 staining showed that cell apoptosis induced by costunolide might be related to DNA damage. The apoptosis mechanism relied on regulating the protein expression of Bax, Bcl-2, p53, Caspase-3 and the activation of p38MAPK and nuclear factor κB (NF-κB) pathways. This study will provide some experimental basis and potential therapeutic strategy for breast cancer treatment.

A study on the protective effects of taxifolin on human umbilical vein endothelial cells and THP-1 cells damaged by hexavalent chromium: a probable mechanism for preventing cardiovascular disease induced by heavy metals.

Hexavalent chromium [Cr(vi)] which is a kind of heavy metal with strong oxidizing ability can induce cardiovascular disease (CVD), while taxifolin can protect cells and organisms against suffering from oxidative stress. In this study, the inhibitory effects of taxifolin against Cr(vi)-induced cell damage in human umbilical vein endothelial cells (HUVECs) and THP-1 cells were investigated. Cr(vi) could increase the phosphorylation of p38 and JNK, regulate the expression of Bax and Bcl-2 in both cell lines. Meanwhile, the Cr(vi) stimulation led to an increase of the expression of ICAM-1 and VCAM-1, and upregulated the adhesion of THP-1 cells to HUVECs. Furthermore, Cr(vi) could induce the activation of the nuclear factor kappa B (NF-κB) signaling pathway, the accumulation of p65 in the nucleus, and the increase in the phosphorylation of IκB and the expression of cleaved caspase-1 and IL-1ß in THP-1 cells. However, taxifolin could reverse the effects by inhibiting the activation of mitogen-activated protein kinases (MAPKs) and NF-κB signaling pathways, regulating the expression of apoptosis-related proteins, and alleviating the adhesion of THP-1 cells to HUVECs. Our findings demonstrated that taxifolin was a potential agent to prevent endothelial dysfunction, monocyte inflammation and cell adhesion induced by Cr(vi).