Oxidative stress plays a critical role in endothelial injury and the pathogenesis of diverse cardiovascular diseases, including atherosclerosis. Isoquercitrin (quercetin-3-glucoside), a flavonoid distributed widely in plants, exhibits many biological activities, including anti-allergic, anti-viral, anti-inflammatory, and anti-oxidative effects. In the present study, the inhibitory effect of isoquercitrin on H2O2-induced apoptosis of EA.hy926 cells was evaluated. MTT assays showed that isoquercitrin significantly inhibited H2O2-induced loss of viability in EA.hy926 cells. Hoechst33342/PI and Annexin V-FITC/PI fluorescent double staining indicated that isoquercitrin inhibited H2O2-induced apoptosis of EA.hy926 cells. Western blotting demonstrated that isoquercitrin prevented H2O2-induced increases in cleaved caspase-9 and cleaved caspase-3 expression, while increasing expression of anti-apoptotic protein Mcl-1. Additionally, isoquercitrin significantly increased the expression of p-Akt and p-GSK3β in a dose-dependent manner in EA.hy926 cells. LY294002, a PI3K/Akt inhibitor, inhibited isoquercitrin-induced GSK3β phosphorylation and increase of Mcl-1 expression, which indicated that regulation of isoquercitrin on Mcl-1 expression was likely related to the modulation of Akt activation. These results demonstrated that the anti-apoptotic effect of isoquercitrin on H2O2-induced EA.hy926 cells was likely associated with the regulation of isoquercitrin on Akt/GSK3β signaling pathway and that isoquercitrin could be used clinically to interfere with the progression of endothelial injury-associated cardiovascular disease.
The vascular endothelium is important in the physiological homeostasis of blood vessels. Increasing evidence demonstrates that oxidative stress‑induced endothelial damage is involved in the pathogenesis of several cardiovascular diseases, including atherosclerosis. Hyperoside, one of major active components from Apocynum venetum L. (Luo‑Bu‑Ma), which is a traditional Chinese herbal medicine commonly used for the prevention of cardiovascular diseases, exhibits diverse bioactivities, including anti‑inflammatory and antioxidant effects. In the present study, the protective effects of hyperoside against hydrogen peroxide (H2O2)‑induced apoptosis of human umbilical vein endothelial cells (HUVECs) were investigated. The results demonstrated that hyperoside significantly prevented the loss of cell viability, the increase of endothelial Ca2+ content and apoptosis in H2O2‑induced HUVECs. Additionally, reverse transcription-polymerase chain reaction and western blot analysis revealed that hyperoside significantly decreased the mRNA expression levels of B‑cell lymphoma (Bcl)‑2 associated X protein (Bax), cleaved caspase‑3 and phosphorylated‑p38, while increasing the mRNA expression of Bcl‑2 in H2O2‑induced HUVECs. The present findings suggested that hyperoside has protective effects against H2O2‑induced apoptosis in HUVECs and serves a key role in the prevention of cardiovascular diseases.
Introduction: Type 2 mellitus (T2DM), a chronic metabolic disorder, causes severe impairment of patients’ quality of life and has attracted global attention. Many studies have suggested the importance of the gut microbiota in the occurrence of T2DM. The Scrophulariae Radix and Atractylodes sinensis (XC) pair, recommended in traditional Chinese medicine (TCM), have been used for treating diabetes for many years. However, research on the role of the XC pair in modulating gut microbial communities is lacking, but it is important to elucidate the underlying mechanism.Methods: In this study, we detected bacterial communities by high-throughput 16S rRNA gene sequencing.Results: The results showed that XC + MET reduced postprandial hyperglycemia and inflammatory response in diabetic rats more effectively than metformin (MET) alone. The XC + MET treatment reshaped the intestinal microbial composition of diabetic rats. XC can help MET regulate carbohydrate, amino acid, and lipid metabolism, particularly the insulin signaling pathway.Discussion: This research would help elucidate potential mechanisms and the treatment methods.
29 February 2016 in International Journal of Molecular Medicine
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