GALLIC ACID IMPROVES OXIDATIVE STRESS AND INFLAMMATION THROUGH REGULATING MICRORNAS EXPRESSIONS IN THE BLOOD OF DIABETIC RATS
- PMID: 31508175
- PMCID: PMC6711635
- DOI: 10.4183/aeb.2019.187
GALLIC ACID IMPROVES OXIDATIVE STRESS AND INFLAMMATION THROUGH REGULATING MICRORNAS EXPRESSIONS IN THE BLOOD OF DIABETIC RATS
Abstract
Context: Endothelial dysfunction and diabetic cardiomyopathy are critical complications of diabetes. Gallic acid (GA) plays a significant role in cardiovascular disorders resulted from diabetes. In addition, increased plasma miR-24, miR-126 associated with endothelial dysfunction.
Aim: The current study was designed to assess the effects of GA on plasma miR-24, miR-126 levels in the diabetic rats.
Animals and methods: Adult male Sprague-Dawley rats were divided into three groups (n=8): control (C), diabetic (D) and diabetic group treated with GA (D+G, 25 mg/kg, by gavage) for eight weeks. The blood glucose level, body weight, lipid profile, blood pressure, plasma miR-24 and miR-126 levels, antioxidant and inflammatory biomarkers were measured.
Results: The plasma levels of miR-24, miR-126, body weight, high-density lipoprotein cholesterol (HDL-c), total anti-oxidant capacity (TAC) and the systolic blood pressure significantly reduced and blood glucose, total cholesterol (TC), triglycerides (TG), very low-density lipoprotein cholesterol (VLDL-c), malondialdehyde (MDA), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α) and low-density lipoprotein cholesterol (LDL-c) significantly elevated among the diabetic rats compared with the control group. However, GA restored body weight, blood pressure, TC, TG, VLDL-c, TNF-α, miR-126, blood glucose, HDL-c, MDA, TAC, miR-24 and IL-6 among the GA treated rats compared with the diabetic group.
Conclusion: GA improves inflammation, oxidative stress and hypotension result from diabetes. These protective effects are probably mediated via increasing plasma miR-24 and miR-126 levels.
Keywords: Diabetes; Endothelium; Gallic acid; MicroRNA.
Conflict of interest statement
The author declared no potential conflict of interest with respect to the research, authorship, and/or publication of this article.
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