Vaccarin protects human microvascular endothelial cells from apoptosis via attenuation of HDAC1 and oxidative stress

  title={Vaccarin protects human microvascular endothelial cells from apoptosis via attenuation of HDAC1 and oxidative stress},
  author={Xuexue Zhu and Yueyue Lei and Fanggen Tan and Leilei Gong and Haifeng Gong and Wei Yang and Ting Chen and Zhixuan Zhang and Weiwei Cai and Bao Hou and Xu Wang and Haijian Sun and Yue-tao Zhou and Liying Qiu},
  journal={European Journal of Pharmacology},

Figures from this paper

Vaccarin prevents ox-LDL-induced HUVEC EndMT, inflammation and apoptosis by suppressing ROS/p38 MAPK signaling.
It is suggested that vaccarin impeded ox-LDL-triggered HUVEC inflammation, EndMT and apoptosis via inhibition of ROS/p38 MAPK signaling pathway and may have a therapeutic effect on endothelial injury-related disorders.
HDAC1: an environmental sensor regulating endothelial function.
The HDAC1-dependent regulation of endothelial function through the deacetylation of both histone and non-histone proteins ultimately impacts whole animal physiology and health.
Cucumis sativus Aqueous Fraction Inhibits Angiotensin II-Induced Inflammation and Oxidative Stress In Vitro
Evaluated subfractions from the Cucumis sativus aqueous fraction showed that C4 has anti-inflammatory and antioxidant effects, and was the most effective combination to inhibit the production of IL-6.
Vaccarin Regulates Diabetic Chronic Wound Healing through FOXP2/AGGF1 Pathways
VAC promoted chronic wound healing in T1DM mice by activating the FOXP2/AGGF1 pathway, indicating that VAC may be a promising candidate for the treatment of the chronic wounds of diabetic patients.
Down-regulated HDAC1 and up-regulated microRNA-124-5p recover myocardial damage of septic mice
This study suggests that down-regulated HDAC1 or up-regulated miR-124-5p recovers myocardial damage of septic mice via decreasing HMGB1.
Chemical Constituents from Albiziae Cortex and Their Ability to Ameliorate Steatosis and Promote Proliferation and Anti-Oxidation In Vitro
This is the first report of the isolation of lignan skeletons from the genus Albizzia julibrissin with the ability to ameliorate steatosis and promote proliferation and anti-oxidation activities.
Vaccarin prevents titanium particle‐induced osteolysis and inhibits RANKL‐induced osteoclastogenesis by blocking NF‐κB and MAPK signaling pathways
It was indicated that vaccarin could effectively inhibit RANKL‐induced osteoclastogenesis, fusion of F‐actin rings, bone resorption, and expression of osteOClast marker genes in a dose‐dependent manner in vitro, and in vivo results showed that Vaccarin exhibited an inhibitory effect on titanium particle‐ induced osteolysis by antiosteoclastogenic.


Vaccarin attenuates the human EA.hy926 endothelial cell oxidative stress injury through inhibition of Notch signaling.
It was found that vaccarin may be able to selectively protect vascular endothelium from dysfunction induced by H2O2, and downregulated caspase-3, a cell apoptotic pathway-related protein.
Vaccarin attenuates high glucose-induced human EA•hy926 endothelial cell injury through inhibition of Notch signaling.
It was found that preincubation with vaccarin protected the EA·hy926 cells from high glucose‑induced cell injury, which promoted cell viability and migratory ability, inhibited the expression levels of LDH and MDA, and enhanced the activity of SOD.
Methylglyoxal‐induced apoptosis is dependent on the suppression of c‐FLIPL expression via down‐regulation of p65 in endothelial cells
MGO was found to induce apoptosis by down‐regulating p65 expression at both the transcriptional and posttranslational levels, and thus, to inhibit c‐FLIPL mRNA expression by suppressing NF‐κB transcriptional activity.
Curcumin attenuates high glucose-induced podocyte apoptosis by regulating functional connections between caveolin-1 phosphorylation and ROS
In diabetic rats, administration of curcumin not only significantly improved the renal function, but also suppressed ROS levels, oxidative stress, apoptosis and cav-1 phosphorylation in the kidneys.
Imeglimin prevents human endothelial cell death by inhibiting mitochondrial permeability transition without inhibiting mitochondrial respiration
It is concluded that Imeglimin prevents hyperglycemia-induced cell death in HMEC-1 through inhibition of PTP opening without inhibiting mitochondrial respiration nor affecting cellular energy status.
Suppression of Excessive Histone Deacetylases Activity in Diabetic Hearts Attenuates Myocardial Ischemia/Reperfusion Injury via Mitochondria Apoptosis Pathway
Suppression of HDACs activity triggered protective effects against MI/R and H/R injury under hyperglycemia conditions through Akt-modulated mitochondrial apoptotic pathways via Foxo3a/Bim.
Salusin-β mediates high glucose-induced endothelial injury via disruption of AMPK signaling pathway.
C1q/TNF-Related Protein-9 Ameliorates Ox-LDL-Induced Endothelial Dysfunction via PGC-1α/AMPK-Mediated Antioxidant Enzyme Induction
It is observed that treatment with ox-LDL inhibited the proliferation, migration, angiogenesis and the generation of NO, while stimulated the apoptosis and reactive oxygen species (ROS) production in HUVECs, providing the first evidence that CTRP9 attenuated ox- LDL-induced endothelial injury by antioxidant enzyme inductions dependent on PGC-1α/AMPK activation.
A novel Osmium-based compound targets the mitochondria and triggers ROS-dependent apoptosis in colon carcinoma
The anticancer activity of a novel Osmium-based organometallic compound (hereafter named Os) on different colorectal carcinoma cell lines is reported with potent anticancer effect in vitro and in vivo, which could have potential implications for strategic therapeutic drug design.
Evaluation of Antioxidant Activities of Ampelopsin and Its Protective Effect in Lipopolysaccharide-Induced Oxidative Stress Piglets
The results of the present investigation suggest that APS possesses a strong antioxidant activity and alleviates LPS-induced oxidative stress, possibly due to its ability to prevent reactive oxygen species.