Literature DB >> 31508175

GALLIC ACID IMPROVES OXIDATIVE STRESS AND INFLAMMATION THROUGH REGULATING MICRORNAS EXPRESSIONS IN THE BLOOD OF DIABETIC RATS.

F Ramezani Ali Akbari1,2, M Badavi1,2,3, M Dianat1,2, S A Mard1,2, A Ahangarpour1,2,4.   

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.

Entities:  

Keywords:  Diabetes; Endothelium; Gallic acid; MicroRNA

Year:  2019        PMID: 31508175      PMCID: PMC6711635          DOI: 10.4183/aeb.2019.187

Source DB:  PubMed          Journal:  Acta Endocrinol (Buchar)        ISSN: 1841-0987            Impact factor:   0.877


  31 in total

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