Authors

  • Guldona Tayirova
    Andijan Branch of Kokand University
  • Toyirjon Saydullaev
    Andijan Branch of Kokand University

DOI:

https://doi.org/10.71337/inlibrary.uz.ijai.115033

Abstract

Atherosclerosis is a widespread and severe systemic disease and remains a leading cause of cardiovascular morbidity and mortality. This study aimed to investigate the effect of the antioxidant dibunol on the serum lipid profile in rabbits with experimentally induced atherosclerosis. The results demonstrated that dibunol significantly reduced serum cholesterol, triglycerides, and beta-lipoprotein levels, confirming its potential for atherosclerosis prevention and therapy.

 

 

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INTERNATIONAL JOURNAL OF ARTIFICIAL INTELLIGENCE

ISSN: 2692-5206, Impact Factor: 12,23

American Academic publishers, volume 05, issue 06,2025

Journal:

https://www.academicpublishers.org/journals/index.php/ijai

page 889

THE EFFECT OF THE ANTIOXIDANT DIBUNOL ON THE LIPID PROFILE OF

BLOOD SERUM IN RABBITS WITH EXPERIMENTAL ATHEROSCLEROSIS

Tayirova Guldona Sanjarbekovna

Student of the 2nd year, Faculty of Medicine, General Medicine Department,

Andijan Branch of Kokand University

Saydullaev Toyirjon

Scientific Advisor: Head of the Department of Medical Biology and Histology, ADTI,

PhD in Medical Sciences, Associate Professor

Abstract:

Atherosclerosis is a widespread and severe systemic disease and remains a leading

cause of cardiovascular morbidity and mortality. This study aimed to investigate the effect of

the antioxidant dibunol on the serum lipid profile in rabbits with experimentally induced

atherosclerosis. The results demonstrated that dibunol significantly reduced serum cholesterol,

triglycerides, and beta-lipoprotein levels, confirming its potential for atherosclerosis prevention

and therapy.

Keywords:

Atherosclerosis, ischemic heart disease, antioxidant, dibunol, lipid metabolism,

cholesterol, triglycerides, beta-lipoproteins, experimental model, prevention.

Relevance of the Study:

Atherosclerosis and its complications, particularly ischemic heart disease, are among the

leading causes of death and disability worldwide [1]. According to WHO, in 2021,

cardiovascular diseases accounted for approximately 20.5 million deaths globally, constituting

nearly one-third of all deaths. Notably, 85% of these were associated with atherosclerotic

cardiovascular conditions. In 2019, cardiovascular diseases caused 107,394 deaths in

Uzbekistan, placing the country among those with the highest mortality rates from such

diseases. Daily smoking prevalence among men stands at 24.1%, a major risk factor for

cardiovascular pathology. Given the disease's significant impact on modern healthcare systems,

especially within the context of Uzbekistan, the development of effective prevention and

treatment methods is imperative. In-depth understanding of the pathogenesis of atherosclerosis

and disorders of lipid metabolism is key to developing effective pharmacological agents. From

this perspective, antioxidants play a crucial role in the prevention of atherosclerosis [2].

Atherosclerosis: Pathogenetic Basis and Clinical Manifestations

Atherosclerosis is a chronic and progressive disease resulting from the accumulation of

cholesterol, lipoproteins (especially LDL), lipids, and mineral substances in arterial walls [6].

These substances damage the endothelium—the inner layer of arteries—undergo oxidation, and


background image

INTERNATIONAL JOURNAL OF ARTIFICIAL INTELLIGENCE

ISSN: 2692-5206, Impact Factor: 12,23

American Academic publishers, volume 05, issue 06,2025

Journal:

https://www.academicpublishers.org/journals/index.php/ijai

page 890

trigger inflammatory responses [3]. Consequently, atheromatous plaques form beneath the

endothelial layer.

Stages of Pathogenesis:

Endothelial Dysfunction: Triggered by risk factors such as smoking, hypertension, and

hyperglycemia, leading to microscopic endothelial injury and infiltration of lipoproteins. Lipid

Accumulation and Oxidation: Low-density lipoproteins (LDL) oxidize within the vascular wall.

Macrophages engulf these oxidized particles, transforming into foam cells. Inflammation:

Monocytes, T-lymphocytes, and inflammatory mediators (e.g., IL-1, TNF-α) amplify the

inflammatory process, promoting plaque growth and complexity [4]. Plaque Complication and

Calcification: Formation of necrotic zones, fibrous collagen layers, and calcium deposits leads

to arterial stiffening and loss of elasticity [5]. Increased Risk of Thrombosis: Plaque rupture

may result in clot formation, leading to acute ischemic events such as myocardial infarction or

stroke.

Clinical Manifestations:

Atherosclerosis affects various vascular beds:Coronary Arteries: Chest pain (angina),

arrhythmias, heart failure [7]. Cerebral Arteries: Headache, visual disturbances, speech

impairment, imbalance, stroke. Peripheral Arteries (Lower Limbs): Claudication, cold

extremities, risk of necrosis. Clinicians distinguish between two stages of the disease:

Asymptomatic (Subclinical) Stage

Manifest (Clinical) Stage – when arterial stenosis becomes significant (>50%), leading to

symptom development.

Materials and Methods:

An experimental model of atherosclerosis was established in laboratory rabbits. Cholesterol

emulsion in cottonseed oil was administered daily via an elastic gastric tube for 30–60 days.

This led to a significant increase in serum levels of cholesterol, triglycerides, and beta-

lipoproteins. Subsequently, rabbits in the experimental group received dibunol at a dose of 30

mg/kg div weight. All biochemical parameters were assessed using standard laboratory

diagnostic techniques.

Results and Discussion:

In rabbits with induced experimental atherosclerosis, serum cholesterol levels were

significantly elevated. Upon administration of dibunol, the following improvements in lipid

parameters were observed: Cholesterol: Decreased from 387.42 mg% to 108.4 mg%.

Triglycerides: Decreased from 947 mg% to 73.7 mg%. Beta-lipoproteins: Decreased from

685.77 mg% to 351.32 mg%. These findings indicate that dibunol significantly attenuates lipid

metabolism disorders, which play a key role in the pathogenesis of atherosclerosis.

Conclusion:


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INTERNATIONAL JOURNAL OF ARTIFICIAL INTELLIGENCE

ISSN: 2692-5206, Impact Factor: 12,23

American Academic publishers, volume 05, issue 06,2025

Journal:

https://www.academicpublishers.org/journals/index.php/ijai

page 891

The results of this experimental study demonstrated that the antioxidant dibunol is effective in

preventing and treating atherosclerosis. It exerts a beneficial effect by lowering serum

cholesterol, triglycerides, and beta-lipoprotein levels, thereby targeting critical components of

atherosclerotic pathogenesis. These findings highlight the potential use of antioxidants in both

the prevention and treatment of atherosclerosis.

Recommendations:

Dibunol may be considered as a supportive agent in the prevention and treatment of

atherosclerosis. Further clinical studies are necessary to evaluate its efficacy and safety in

humans. Moreover, incorporating antioxidant-rich foods into the daily diet and developing

antioxidant-based therapeutic strategies for patients with atherosclerosis are highly

recommended.

References:

1. Ross, R. (1999). Atherosclerosis - an inflammatory disease. New England Journal of

Medicine, 340(2), 115–126.
2. Libby, P. (2002). Inflammation in atherosclerosis. Nature, 420(6917), 868–874.
3. Ross, R. (1999). Atherosclerosis—An Inflammatory Disease. New England Journal of

Medicine, 340(2), 115–126. doi:10.1056/NEJM199901143400207
4. Libby, P., Ridker, P.M., Hansson, G.K. (2011). Inflammation in Atherosclerosis: From

Pathophysiology to Practice. Journal of the American College of Cardiology, 54(23), 2129–

2138. doi:10.1016/j.jacc.2009.09.009
5. Kumar, V., Abbas, A.K., Aster, J.C. (2020). Robbins & Cotran Pathologic Basis of Disease.

10th Ed. Elsevier.
6. Jo‘raqulov, Sh.R., Alimov, A.A. Propedeutics of Internal Diseases. – Tashkent: “Tibbiyot”

Publishing, 2018. – p. 420.
7. Mamatqulov, A., Yusupova, M.X. Clinical Therapy: Cardiovascular Diseases. – Tashkent:

“Science and Technology”, 2020. – p. 368.

References

Ross, R. (1999). Atherosclerosis - an inflammatory disease. New England Journal of Medicine, 340(2), 115–126.

Libby, P. (2002). Inflammation in atherosclerosis. Nature, 420(6917), 868–874.

Ross, R. (1999). Atherosclerosis—An Inflammatory Disease. New England Journal of Medicine, 340(2), 115–126. doi:10.1056/NEJM199901143400207

Libby, P., Ridker, P.M., Hansson, G.K. (2011). Inflammation in Atherosclerosis: From Pathophysiology to Practice. Journal of the American College of Cardiology, 54(23), 2129–2138. doi:10.1016/j.jacc.2009.09.009

Kumar, V., Abbas, A.K., Aster, J.C. (2020). Robbins & Cotran Pathologic Basis of Disease. 10th Ed. Elsevier.

Jo‘raqulov, Sh.R., Alimov, A.A. Propedeutics of Internal Diseases. – Tashkent: “Tibbiyot” Publishing, 2018. – p. 420.

Mamatqulov, A., Yusupova, M.X. Clinical Therapy: Cardiovascular Diseases. – Tashkent: “Science and Technology”, 2020. – p. 368.