Related Experiment Video

Updated: Jan 3, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

819

Icariin reduces high glucose-induced endothelial progenitor cell dysfunction via inhibiting the p38/CREB pathway and

Sisi Chen1,2,3, Zhenya Wang1,2,3, Heng Zhou1,2,3

  • 1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.

Experimental and Therapeutic Medicine
|November 28, 2019
PubMed

Insights

Icariin improves high glucose-induced endothelial progenitor cell (EPC) dysfunction by inhibiting the p38/CREB pathway and activating the Akt/eNOS/NO pathway. This natural compound shows potential for treating conditions involving impaired EPC function.

Area of Science:

  • Cardiovascular Biology
  • Cellular and Molecular Medicine
  • Pharmacology and Therapeutics

Background:

  • High glucose (HG) negatively impacts endothelial progenitor cell (EPC) function, a critical process in vascular health.
  • The p38 mitogen-activated protein kinase pathway activation and Akt/endothelial nitric oxide (NO) synthase (eNOS)/NO pathway inhibition are key mechanisms in HG-induced EPC dysfunction.
  • Icariin, a natural compound, has demonstrated protective effects on endothelial cells.

Purpose of the Study:

  • To investigate the therapeutic effects of icariin on high glucose-induced dysfunction in EPCs.
  • To assess icariin's impact on EPC proliferation, migration, and tube formation.
  • To elucidate the molecular mechanisms underlying icariin's protective actions on EPCs.

Main Methods:

  • Endothelial progenitor cells (EPCs) were isolated from Sprague-Dawley rats and treated with high glucose in vitro.
  • The effects of varying icariin concentrations on EPC proliferation, migration, and tube formation were evaluated.
  • Western blotting was used to analyze the phosphorylation status of p38, cAMP response element binding protein (CREB), Akt, and eNOS.
  • Nitric oxide (NO) production was measured to assess pathway activation.

Main Results:

  • Icariin dose-dependently reversed HG-induced inhibition of EPC proliferation, with maximal efficacy at 1 µM.
  • A concentration of 1 µM icariin partially restored HG-impaired EPC migration and tube formation.
  • Icariin significantly suppressed HG-induced p38 and CREB phosphorylation while increasing Akt and eNOS activation.
  • Icariin treatment led to increased NO production in EPCs.

Conclusions:

  • Icariin effectively attenuates high glucose-induced endothelial progenitor cell dysfunction.
  • The protective effects of icariin are partly mediated by inhibiting the p38/CREB pathway.
  • Icariin promotes EPC function through the activation of the Akt/eNOS/NO pathway.
  • Icariin presents a potential therapeutic candidate for conditions characterized by impaired EPC function.

Keywords:
endothelial progenitor cellicariinmigrationproliferationtube formation

More Related Videos

A Method for Mouse Pancreatic Islet Isolation and Intracellular cAMP Determination12:33

A Method for Mouse Pancreatic Islet Isolation and Intracellular cAMP Determination

Published on: June 25, 2014

66.0K
Author Spotlight: Network Pharmacology and Molecular Docking to Decipher the Action of Jiawei Shengjiang San Against Diabetic Kidney Disease08:15

Author Spotlight: Network Pharmacology and Molecular Docking to Decipher the Action of Jiawei Shengjiang San Against Diabetic Kidney Disease

Published on: May 10, 2024

877

Related Concept Videos

cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
8.1K
Cell Specific Gene Expression01:58

Cell Specific Gene Expression

Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...
16.1K
Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a...
521
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
7.1K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
5.2K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
5.5K