Abstract
Effects of mulberry leaf-related extracts (MLREs) on hydrogen peroxide-induced DNA damage in human lymphocytes and on inflammatory signaling pathways in human aortic endothelial cells (HAECs) were studied. The tested MLREs were rich in flavonols, especially bombyx faces tea (BT) in quercetin and kaempferol. Polyphenols, flavonoids, and anthocyanidin also abounded in BT. The best trolox equivalent antioxidant capacity (TEAC) was generated from the acidic methanolic extracts of BT. Acidic methanolic and water extracts of mulberry leaf tea (MT), mulberry leaf (M), and BT significantly inhibited DNA oxidative damage to lymphocytes based on the comet assay as compared to the H2O2-treated group. TNF-α-induced monocyte-endothelial cell adhesion was significantly suppressed by MLREs. Additionally, nuclear factor kappa B (NF-κB) expression was significantly reduced by BT and MT. Significant reductions were also observed in both NF-κB and activator protein (AP)-1 DNA binding by MLREs. Significant increases in peroxisome proliferator-activated receptor (PPAR) α and γ DNA binding by MLREs were also detected in M and MT extracts, but no evidence for PPAR α DNA binding in 50 μg/mL MT extract was found. Apparently, MLREs can provide distinct cytoprotective mechanisms that may contribute to its putative beneficial effects on suppressing endothelial responses to cytokines during inflammation.
Highlights
Atherosclerosis is a chronic inflammatory process characterized by increased oxidative stress [1]
bombyx faces tea (BT) had a higher trolox equivalent antioxidant capacity (TEAC) value (155.14 mM, Table 3) than the TEAC values of 4.7 mM [42] and 6.4 mM [43] reported for quercetin, as well as 2.42 mM reported for quercetin-3rutinoside [44]
Our results suggest that mulberry leaf-related extracts (MLREs) and aspirin significantly inhibited TNF-α-induced monocyteendothelial cell adhesion (Figure 3)
Summary
Atherosclerosis is a chronic inflammatory process characterized by increased oxidative stress [1]. Inflammatory cytokines, tumor necrosis factor-alpha (TNF-α), nuclear factor kappa B (NF-κB), and activator protein (AP)-1 are the major redox-sensitive eukaryotic transcription factors that regulate the expression of adhesion molecules [3, 4]. Because the activation of NF-κB and AP-1 can be inhibited to various degrees by different antioxidants, endogenous reactive oxygen species (ROS) may play an important role in these redoxsensitive transcription pathways in atherogenesis [1, 5]. Nuclear receptors such as glucocorticoid, estrogen, peroxisome proliferator-activated receptors (PPARs), and liver X receptors negatively modulate inflammatory responses by downregulation of AP-1 and NF-κB [6,7,8]. A number of phytochemicals commonly used in research have antioxidant activity that can protect cells from ROS-mediated DNA damage that results in mutation and subsequent carcinogenesis [11]. Several herbs are consumed to protect against common and serious diseases such as cardiovascular and cerebrovascular events, cancer, and other age-related degenerative diseases as well [13]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
