Cardioprotective Effect of Nicorandil, a Mitochondrial ATP-Sensitive Potassium Channel Opener, Prolongs Survival in HSPB5 R120G Transgenic Mice
2011

Nicorandil Prolongs Survival in Mice with Heart Disease

Sample size: 19 publication 10 minutes Evidence: moderate

Author Information

Author(s): Sanbe Atsushi, Marunouchi Tetsuro, Yamauchi Junji, Tanonaka Kouichi, Nishigori Hideo, Tanoue Akito

Primary Institution: Iwate Medical University

Hypothesis

Does nicorandil protect against mitochondrial dysfunction and apoptosis in HSPB5 R120G transgenic mice?

Conclusion

Nicorandil may prolong survival in HSPB5 R120G transgenic mice by protecting against mitochondrial impairments.

Supporting Evidence

  • Nicorandil treatment reduced mitochondrial impairment in mice.
  • Apoptotic cell death was inhibited by nicorandil in cardiomyocytes.
  • Survival rates improved in R120G transgenic mice treated with nicorandil.
  • Nicorandil blocked the release of cytochrome c from mitochondria.
  • Alterations in BCL2 and BAX levels were observed with nicorandil treatment.

Takeaway

Nicorandil is a medicine that helps mice with heart problems live longer by protecting their heart cells from damage.

Methodology

The study involved treating HSPB5 R120G transgenic mice with nicorandil and analyzing its effects on mitochondrial function and apoptosis.

Potential Biases

Potential bias due to funding from a pharmaceutical company involved in the study.

Limitations

The study primarily focused on a specific mouse model and may not directly translate to human conditions.

Participant Demographics

HSPB5 R120G transgenic mice were used in the study.

Statistical Information

P-Value

p<0.05

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pone.0018922

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