Coronary heart disease (CHD) is the cardiovascular disease with
the highest death rate in the world. Several factors that influence Coronary Heart
Disease include the inflammatory process and prolonged oxidative stress.
Enalapril is an ACEI class of drug that has been proven and is widely used to
inhibit myocardial fibrosis and ventricular remodeling. Antioxidants and antiinflammatories
are substances that can reduce oxidative stress and inflammation,
one of which is Black Cumin which contains compounds Thymoquinone (TQ).
This study tested the use Thymoquinon as a potential therapy to treat fibrosis and
cardiac changes following myocardial infarction, Objective: To determine the
effect of Thymoquinone in inhibiting myocardial fibrosis after myocardial
infarction, and to analyze the effect of Thymoquinone on the expression of proinflammatory
cytokines in the serum of Sprague Dawley rats model of myocardial
infarction.
Methods : The type of research used was experimental, using male white rats
(Spraque dawley) as experimental animals. The research design used was a
completely randomized design, post test only control group design. This research
was carried out over a period of 7 days. A total of 30 male white mice aged 3-4
months weighed 200 - 300 grams. All mice were made to develop myocardial
infarction by being given an intraperitoneal injection of LPS 15 mg/kg BW. Mice
were divided into seven groups. Each group consisted of five mice. Then given
treatment for 7 days. Left ventricular tissue was taken for ELISA examination of
MDA, CRP, TNF-α, TGF-β, IL-6 and immunohistochemical examination of
MDA, TNF-α, TGF-β. Troponin and histopathology. Immunohistochemistry and
histology examinations were carried out by two anatomical pathologists.
Results : Our research shows that therapy with Enalapril, Thymoquinone, or a
combination of both succeeded in reducing the levels of IL-6, MDA, TNF-α, CRP
and MDA, CRP, TNF-α, TGF-β in myocardial infarction model mice even lower
and significantly different (p < 0>that the condition becomes similar to the normal control group. therapy reduced
Troponin levels and cardiac fibrosis to be comparable to the normal group
(p<0>inflammation and heart damage in myocardial infarction mice.
Conclusion : Administration of Thymoquinone can inhibit the formation of
myocardial fibrosis after myocardial infarction, but administration of
Thymoquinone has a significant effect on reducing the levels of IL-6, MDA, TNF-
α, TGF-β, CRP, TnI, and the extent of myocardial fibrosis in the serum of Sprague
Dawley rats model of myocardial infarctio.