Abstract

The prevalence of diabetes mellitus (DM) is increasing. DM can cause an imbalance between protective antioxidants and increased production of free radicals. One such antioxidant is the endogenous enzyme glutathione peroxidase (GPx). Kersen (Muntingia calabura L.) contains flavonoids which show antioxidant activity. The purpose of this study was to examine the potential antioxidant of Kersen Leaves (Muntingia Calabura L.) leaves to GPx Enzymes in Diabetic Rats. This research is included in an experimental study with a post-test design only with control category design. The subjects of this study were 36 male rats. The measure of GDP levels using the GOD-PAP enzymatic method, while GPx uses the UV method. Data were analyzed using paired-t-test and OneWay ANOVA test. Statistical test results with paired t test showed significant differences in GDP levels before and after treatment (p = 0.0001). In the OneWay ANOVA test there was a average different GPx levels in each category (p = 0.0001). The most effective steeping increases the GPx level is a dose of 750 mg / 200 gr BW.

Highlights

  • Diabetes mellitus (DM) is one of the public health problems

  • This research is an experimental study to test the effectiveness of steeping leaves of kersen (Muntingia calabura L.) on the level of glutathione peroxidase (GPx) in diabetes mellitus rat induced by Streptozotocin-nicotinamide (STZ-Na) with post-test only with control category design. design

  • GPx levels in the treatment groups P1 (250 mg/Kg BW), P2 (500 mg/ Kg BW) and P3 (750 mg/Kg BW) had an increase compared to the negative control category and approached the positive and control categories

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Summary

Introduction

Diabetes mellitus (DM) is one of the public health problems. According to the results of DM epidemiological studies, Indonesian population aged over 15 years shows a prevalence of 1.5-2.3% [1,2]. An increase in blood sugar or hyperglycemia results in glucose auto-oxidation, protein glycation, and activation of the polyol metabolic pathway which further acceleracers the formation of reactive oxygen compounds. Formation of reactive oxygen compounds can increase lipid, DNA, and protein modification in various tissues. Molecular modification in these tissues results in an imbalance between protective antioxidants (antioxidant defenses) and increased production of free radicals. This is the beginning of oxidative damage known as oxidative stress. Other alternatives are needed to reduce the oxidative damage [7,8,9]

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