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The JAK-STAT Signaling Pathway01:20

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Related Experiment Video

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Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
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SHP-1/STAT3 Interaction Is Related to Luteolin-Induced Myocardial Ischemia Protection.

Donghai Liu1, Hong Luo1, Chenhui Qiao2,3

  • 1Cardiovascular Surgery II, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China.

Inflammation
|August 30, 2021
PubMed
Summary

Luteolin (Lut) protects the heart from ischemia/reperfusion (I/R) injury by reducing myocardial infarction (MI) area and inflammation. This study reveals Lut mediates protection via the SHP-1/STAT3 pathway, offering a potential therapeutic strategy for heart disease.

Keywords:
Hypoxia/Reoxygenation Injury;Ischemia/Reperfusion Injury;Luteolin;Myocardial Ischemia;SHP-1;STAT3.

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Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Pharmacology

Background:

  • Myocardial ischemia/reperfusion (I/R) injury is a critical complication in coronary heart disease surgery.
  • Luteolin (Lut), a flavonoid, exhibits antioxidant properties, but its precise mechanism in I/R injury remains unclear.
  • Investigating Lut's role in I/R injury is crucial for developing effective therapeutic interventions.

Purpose of the Study:

  • To elucidate the protective role of luteolin (Lut) in myocardial ischemia/reperfusion (I/R) injury.
  • To investigate the underlying mechanism involving the Src homology 2 domain-containing protein tyrosine phosphatase 1 (SHP-1)/Signal transducer and activator of transcription 3 (STAT3) pathway.
  • To evaluate the effects of Lut on cardiac function, cell death, and inflammation in I/R models.

Main Methods:

  • Established I/R rat models by ligating and re-perfusing the left anterior descending artery in Lut-pretreated rats.
  • Created hypoxia/reoxygenation (H/R) cell models using H9c2 cells treated with Lut.
  • Assessed infarct area, cardiac function (LVEF), cell apoptosis, inflammatory cytokines, and SHP-1/STAT3 pathway activation via western blotting.

Main Results:

  • Lut treatment significantly reduced myocardial infarction area and improved left ventricular ejection fraction (LVEF) in I/R rats.
  • Lut decreased apoptosis and pro-inflammatory cytokine levels in both I/R rats and H/R cells.
  • Lut downregulated SHP-1 expression and upregulated STAT3 phosphorylation, indicating pathway mediation.

Conclusions:

  • Luteolin demonstrates significant cardioprotective effects against myocardial infarction and I/R injury.
  • The protective mechanism of Lut involves the modulation of the SHP-1/STAT3 signaling pathway.
  • Lut holds promise as a therapeutic agent for mitigating I/R-induced cardiac damage and inflammation.