Volume 35, Issue 2 (May 2024)
Studies in Medical Sciences 2024, 35(2): 126-135 |
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Assistant Professor, Department of Physiology, Faculty of Medicine, Hamedan University of Medical Sciences, Hamedan, Iran (Corresponding Author) , f.ramezani@umsha.ac.ir
Abstract: (1390 Views)
Background & Aim: Aging is associated with dyslipidemia, cardiac hypertrophy and heart damage. Gallic acid has been introduced as an effective agent in improving cardiovascular disorders. In the present study, we demonstrated the protective effects of oral Gallic acid consumption on dyslipidemia and cardiac hypertrophy as well as markers of cardiac damage (lactate dehydrogenase and cardiac creatine kinase).
Materials & Methods: In this experimental study, 32 male Wistar rats were randomly divided into four groups (eight rats in each group): control, control treated with Gallic acid at a dose of 25 mg/kg through gavage for eight weeks, aged rats induced by D-galactose at a dose of 150 mg/kg via intraperitoneal injection for eight weeks without treatment, aged rats induced by D-galactose and treated with Gallic acid. Aging occurred in groups 3 and 4. Cardiac hypertrophy, biochemical factors, and lipid profile were evaluated. One-Way ANOVA was used to compare between groups. SPSS software version 26 was used for statistical calculation. P<0.05 was considered significant.
Results: Aged rats induced with D-galactose showed cardiac hypertrophy compared to the control group (p < 0.01), which was associated with dyslipidemia and increased heart damage markers including lactate dehydrogenase (LDH) (p < 0.001) and Cardiac creatine kinase (CK-MB) (p < 0.05) was associated. Treatment with Gallic acid improved cardiac hypertrophy (p < 0.05), CHOL, LDL (p < 0.001), LDH (p < 0.001) and CK-MB (p < 0.01) in aged rats.
Conclusion: Our study showed that Gallic acid can be introduced as a therapeutic target in heart problems associated with aging. However, more studies with a larger sample size are needed.
Materials & Methods: In this experimental study, 32 male Wistar rats were randomly divided into four groups (eight rats in each group): control, control treated with Gallic acid at a dose of 25 mg/kg through gavage for eight weeks, aged rats induced by D-galactose at a dose of 150 mg/kg via intraperitoneal injection for eight weeks without treatment, aged rats induced by D-galactose and treated with Gallic acid. Aging occurred in groups 3 and 4. Cardiac hypertrophy, biochemical factors, and lipid profile were evaluated. One-Way ANOVA was used to compare between groups. SPSS software version 26 was used for statistical calculation. P<0.05 was considered significant.
Results: Aged rats induced with D-galactose showed cardiac hypertrophy compared to the control group (p < 0.01), which was associated with dyslipidemia and increased heart damage markers including lactate dehydrogenase (LDH) (p < 0.001) and Cardiac creatine kinase (CK-MB) (p < 0.05) was associated. Treatment with Gallic acid improved cardiac hypertrophy (p < 0.05), CHOL, LDL (p < 0.001), LDH (p < 0.001) and CK-MB (p < 0.01) in aged rats.
Conclusion: Our study showed that Gallic acid can be introduced as a therapeutic target in heart problems associated with aging. However, more studies with a larger sample size are needed.
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