| dc.description.abstract | Hyperuricemia can induce a dysfunctional exchange of sodium and calcium in
mitochondria which will lead to the production of reactive oxygen species (ROS).
ROS plays a role in aging, DNA damage, oxidation, production of inflammatory
cytokines, and cell apoptosis. Uric acid metabolism is catalyzed by xanthine
oxidase (XO) to produce hydrogen peroxide (H2O2) which can form scar tissue in
the liver. Alt1 and Hgf expression plays a role in reflecting hepatic cell damage
and repair. Method: true experimental, post-test control group design using stored
biological material (BBT) of 32 samples consisting of four groups, K0: the control
group without treatment; P1: intervention group of 86% fructose and 0.5% CMC;
P2: intervention group of 86% fructose and allopurinol; P3: intervention group of
86% fructose and ethanol extract of melinjo peel. Alt1 and Hgf expression
determination using real-time PCR (rt-PCR) with Livak method 2– Ct. Result:
Alt1 expression in hyperuricemia model rats after 10 days of treatment with
ethanol extract of melinjo peel was lower than the control group (p=0.001), CMC
(p=0.001), and allopurinol (p=0.059). Hgf expression tends to have the same
cycling threshold in all groups (p=0.065). There was no correlation between Alt1
expression and hgf after 10 days of treatment (r=-0.08; p=0.661). Conclusion: the
ethanol extract of melinjo peel has the potential to be a hepato-protector in the
hyperuricemia model rat by reducing Alt1 expression better than the other
treatment groups. | en_US |
