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Fenofibrate improves vascular endothelial function and contractility in diabetic mice.

Nan Xu1, Qin Wang1, Shan Jiang1

  • 1Department of Physiology, School of Basic Medical Sciences, and Kidney Disease Center of First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China.

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|October 9, 2018
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Summary

Fenofibrate improves vascular endothelial function in diabetes by increasing nitric oxide and reducing vasoconstrictors. This balances blood vessel relaxation and contraction, mitigating diabetic vascular complications.

Keywords:
DiabetesEndothelial dysfunctionFenofibrateNitric oxideOxidative stress

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Area of Science:

  • Cardiovascular Research
  • Metabolic Disorders
  • Pharmacology

Background:

  • Diabetic vascular complications are a major health concern.
  • Fenofibrate, a PPARα agonist, shows promise in reducing these complications.
  • The precise mechanisms underlying fenofibrate's protective effects remain unclear.

Purpose of the Study:

  • To investigate if fenofibrate improves endothelial dysfunction in diabetes mellitus (DM).
  • To determine fenofibrate's role in balancing aortic endothelium-dependent relaxation and contractility.
  • To elucidate the molecular pathways involved in fenofibrate's vascular protective effects.

Main Methods:

  • Streptozotocin-induced diabetic mice model.
  • Eight weeks of fenofibrate treatment (100 mg/Kg/d).
  • Assessment of endothelium-dependent relaxation, nitric oxide (NO) levels, renal damage markers, and vasoconstrictor prostaglandin effects.
  • Measurement of oxidative stress markers (superoxide dismutase, catalase, hydrogen peroxide).
  • Inhibition studies using PPARα and AMPKα inhibitors.
  • Western blot analysis for PPARα, LKB1, AMPKα, eNOS, NF-κB p65, and COX-2.
  • In vitro incubation with indomethacin.

Main Results:

  • Fenofibrate improved endothelium-dependent relaxation and increased NO levels in diabetic mice.
  • Fenofibrate treatment reduced renal damage markers and vasoconstrictor prostaglandin effects.
  • Oxidative stress markers were normalized by fenofibrate.
  • Vasodilation was reversed by PPARα or AMPKα inhibitors, indicating pathway involvement.
  • Fenofibrate increased PPARα expression, promoted LKB1 translocation, and activated AMPKα/eNOS signaling.
  • NF-κB p65 and COX-2 protein levels were decreased by fenofibrate.
  • In vitro indomethacin improved aortic contractility.

Conclusions:

  • Fenofibrate normalizes endothelial function in diabetic mice by balancing vascular reactivity.
  • The mechanism involves increased NO production and suppression of vasoconstrictor prostaglandins.
  • Fenofibrate's action is mediated via the PPARα/AMPKα/eNOS pathway.
  • These findings suggest fenofibrate's potential in managing diabetic vascular complications.