Interplay of N- acetyl cysteine and melatonin in regulating oxidative stress-induced cardiac hypertrophic factors and microRNAs

Tahir Ali, Iram Mushtaq*, Sonia Maryam, Anam Farhan, Kiran Saba, Muhammad Ishtiaq Jan, Aneesa Sultan, Mariam Anees, Burcu Duygu, Sadia Hamera, Sobia Tabassum, Qamar Javed, Paula A. da Costa Martin*, Iram Murtaza

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

24 Citations (Web of Science)

Abstract

Early and specific diagnosis of oxidative stress linked diseases as cardiac heart diseases remains a major dilemma for researchers and clinicians. MicroRNAs may serve as a better tool for specific early diagnostics and propose their utilization in future molecular medicines. We aimed to measure the microRNAs expressions in oxidative stress linked cardiac hypertrophic condition induced through stimulants as Endothelin and Isoproterenol. Cardiac hypertrophic animal models were confirmed by BNP, GATA4 expression, histological assays, and increased cell surface area. High oxidative stress (ROS level) and decreased antioxidant activities were assessed in hypertrophied groups. Enhanced expression of miR-152, miR-212/132 while decreased miR-142-3p expression was observed in hypertrophic condition. Similar pattern of these microRNAs was detected in HL-1 cells treated with H2O2. Upon administration of antioxidants, the miRNAs expression pattern altered from that of the cardiac hypertrophied model. Present investigation suggests that oxidative stress generated during the cardiac pathology may directly or indirectly regulate anti-hypertrophy pathway elements through microRNAs including antioxidant enzymes, which need further investigation. The down-regulation of free radical scavengers make it easier for the oxidative stress to play a key role in disease progression.

Original languageEnglish
Pages (from-to)56-65
Number of pages10
JournalArchives of Biochemistry and Biophysics
Volume661
DOIs
Publication statusPublished - Jan 2019

Keywords

  • Cardiac hypertrophy
  • Oxidative stress
  • miRNAs
  • Endothelin
  • Isoproterenol
  • APOPTOSIS
  • HEART
  • EXPRESSION
  • PROTEIN
  • LEAD

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