Ratih Tri Kusuma Dewi, Doctoral Program of Medical Sciences, Faculty of Medicine, Sebelas Maret University, Surakarta, Indonesia, 57126Follow
Bambang Purwanto, Department of Internal Medicine, Dr. Moewardi Hospital, Faculty of Medicine Sebelas Maret University, Surakarta, Indonesia, 57126
Brian Wasita, Department of Pathological Anatomy, Dr. Moewardi Hospital, Faculty of Medicine Sebelas Maret University, Surakarta, Indonesia, 57126
Vitri Widyaningsih, Department of Public Health, Faculty of Medicine Sebelas Maret University, Surakarta, Indonesia, 57126

Background: Prolonged exposure of peritoneal membrane to dialysate solution is known to cause fibrosis mediated by imbalanced inflammatory response and oxidative stress. In this context, proinflammatory cytokines including TGF-β and IL-1β, along with oxidative stress markers namely SOD and MDA, present in circulation, could serve as indicators of fibrosis. This phenomenon has the potential to interfere with the optimization of Chronic Kidney Disease (CKD) treatment. Other oral antioxidant supplements have been widely studied to prevent peritoneal damage, but investigations regarding Astaxanthin (AST) effect on fibrosis marked with proinflammatory cytokine are still limited.

Aims: This study aimed to investigate the protective role of AST supplementation against fibrosis in peritoneal dialysis by evaluating proinflammatory cytokine levels.

Results: The results showed that AST supplementation reduced the levels of MDA, TGF-β, and IL-1β within the circulation while also improving SOD concentration in peritoneal dialysis-induced rats, as indicated by p

Conclusion: This study found that AST supplementation might prevent peritoneal fibrosis by decreasing MDA, TGF-β, and IL-1β, as well as increasing SOD levels in serum.

Dewi, Ratih Tri Kusuma; Purwanto, Bambang; Wasita, Brian; and Widyaningsih, Vitri (2025) "The Protective Role of Astaxanthin Against Oxidative Stress and Inflammation in Peritoneal Dialysis Rats," BioMedicine: Vol. 15 : Iss. 2 , Article 1.
DOI: 10.37796/2211-8039.1651

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