Suppression of apoptosis in vascular endothelial cell, the promising way for natural medicines to treat atherosclerosis

Pharmacol Res. 2021 Jun:168:105599. doi: 10.1016/j.phrs.2021.105599. Epub 2021 Apr 7.

Abstract

Atherosclerosis, a chronic multifactorial disease, is closely related to the development of cardiovascular diseases and is one of the predominant causes of death worldwide. Normal vascular endothelial cells play an important role in maintaining vascular homeostasis and inhibiting atherosclerosis by regulating vascular tension, preventing thrombosis and regulating inflammation. Currently, accumulating evidence has revealed that endothelial cell apoptosis is the first step of atherosclerosis. Excess apoptosis of endothelial cells induced by risk factors for atherosclerosis is a preliminary event in atherosclerosis development and might be a target for preventing and treating atherosclerosis. Interestingly, accumulating evidence shows that natural medicines have great potential to treat atherosclerosis by inhibiting endothelial cell apoptosis. Therefore, this paper reviewed current studies on the inhibitory effect of natural medicines on endothelial cell apoptosis and summarized the risk factors that may induce endothelial cell apoptosis, including oxidized low-density lipoprotein (ox-LDL), reactive oxygen species (ROS), angiotensin II (Ang II), tumor necrosis factor-α (TNF-α), homocysteine (Hcy) and lipopolysaccharide (LPS). We expect this review to highlight the importance of natural medicines, including extracts and monomers, in the treatment of atherosclerosis by inhibiting endothelial cell apoptosis and provide a foundation for the development of potential antiatherosclerotic drugs from natural medicines.

Keywords: (-)-Epigallocatechin-3-gallate (PubChem CID: 65064); 2,3,5,4’-tetrahydroxystilbene-2-O-β-D-glucoside (PubChem CID: 6438627); 3β-Hydroxyolean-12-en-28-oic acid (PubChem CID: 3010929); 6-Shogaol (PubChem CID: 5281794); Akebia Saponin D (PubChem CID: 14284436); Allicin (PubChem CID: 65036); Apigenin (PubChem CID: 5280443); Apoptosis; Atherosclerosis; Blueberry anthocyanin (PubChem CID: 135327637); Capsaicin (PubChem CID: 1548943); Catalpol (PubChem CID: 91520); Celastrol (PubChem CID: 122724); Chicoric acid (PubChem CID: 5281764); Cinnamaldehyde (PubChem CID: 637511); Cyanidin (PubChem CID: 128861); Cyanidin-3-O-β-glucoside (PubChem CID: 441667); Cycloartenyl ferulate (PubChem CID: 5282164); Dihydromyricetin (PubChem CID: 161557); Dioscin (PubChem CID: 119245); Elatoside C (PubChem CID: 101658259); Ellagic acid (PubChem CID: 5281855); Farrerol (PubChem CID: 91144); Folic acid (PubChem CID: 135398658); Genistein (PubChem CID: 5280961); Ginkgolide B (PubChem CID: 65243); Ginsenoside Rb1 (PubChem CID: 9898279); Ginsenoside compound K (PubChem CID: 9852086); Gypenoside XVⅡ (PubChem CID: 11968565); Hyperin (PubChem CID: 5281643); Isoquercitrin (PubChem CID: 5280804); Kaempferol (PubChem CID: 5280863); Ligustrazine (PubChem CID: 14296); Lunasin (PubChem CID: 20054959); Lycopene (PubChem CID: 446925); Myricitrin (PubChem CID: 5281673); Naringenin (PubChem CID: 932); Natural medicines; Notoginsenoside Fc (PubChem CID: 75412556); Notoginsenoside R1 (PubChem CID: 441934); Oxymatrine (PubChem CID: 114850); Paeoniflorin (PubChem CID: 442534); Paeonol (PubChem CID: 11092); Peonidin-3-O-β-glucoside (PubChem CID: 14311151); Picroside Ⅱ (PubChem CID: 11944602); Pinocembrin (PubChem CID: 68071); Protocatechuic Aldehyde (PubChem CID: 528594); Quercetin (PubChem CID: 5280343); Resveratrol (PubChem CID: 445154); Rhein (PubChem CID: 10168); Safflor yellow B (PubChem CID: 131751452); Schisandrin B (PubChem CID: 108130); Scutellarin (PubChem CID: 185617); Vaccarin (PubChem CID: 71307582); Vascular endothelial cells; α-Zearalanol (PubChem CID: 2999413).

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Atherosclerosis / drug therapy*
  • Clinical Trials as Topic
  • Endothelial Cells / drug effects*
  • Endothelial Cells / pathology
  • Humans
  • Lipoproteins, LDL / toxicity
  • Plant Extracts / pharmacology*
  • Plant Extracts / therapeutic use
  • Reactive Oxygen Species / metabolism
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Lipoproteins, LDL
  • Plant Extracts
  • Reactive Oxygen Species
  • Tumor Necrosis Factor-alpha
  • oxidized low density lipoprotein