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Berberine attenuates sunitinib-induced cardiac dysfunction by normalizing calcium regulation disorder via SGK1

Congxin Li1, Wenting Wu2, Jiahui Xing2

  • 1Department of Pharmacy, The Third Hospital of Hebei Medical University, Shijiazhuang, 050051, China.

Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association
|March 27, 2023
PubMed

Insights

Berberine (BBR) protects against Sunitinib (SNT)-induced cardiotoxicity by normalizing calcium regulation. BBR activates serum and glucocorticoid-regulated kinase 1 (SGK1), mitigating heart dysfunction caused by SNT.

Area of Science:

  • Cardiology
  • Pharmacology
  • Molecular Biology

Background:

  • Sunitinib (SNT) causes cardiotoxicity through impaired calcium regulation.
  • Berberine (BBR) is a natural compound with known cardioprotective and calcium-regulating properties.

Purpose of the Study:

  • To investigate if BBR ameliorates SNT-induced cardiotoxicity by restoring calcium homeostasis via SGK1 activation.

Main Methods:

  • Utilized mouse models, neonatal rat cardiomyocytes (NRVMs), and human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs).
  • Assessed cardiac function, calcium transients, contraction, and SERCA2a expression.
  • Investigated the role of SGK1 by using SGK1 inhibitors.

Main Results:

  • BBR prevented SNT-induced cardiac dysfunction, QT prolongation, and histopathological damage in mice.
  • BBR counteracted SNT's inhibition of cardiomyocyte calcium transients and contraction.
  • BBR's protective effects were dependent on SGK1 activation, as shown by experiments with SGK1 inhibitors.

Conclusions:

  • Berberine attenuates Sunitinib-induced cardiotoxicity.
  • The mechanism involves normalizing calcium regulation through the activation of SGK1.
Keywords:
BerberineCardiac contractile dysfunctionHuman-induced pluripotent stem cell-derived cardiomyocytePhosphoinositide 3-kinaseSerum and glucocorticoid-regulated kinase 1Sunitinib

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