Background: Iron overload which accumulates in the body due to repeated blood transfusions in β-thalassemia major patients can cause damage to many organs, especially the liver. Iron overload can be reduced by iron chelating agents. Mangiferin from natural sources has been proven to have the ability as an iron chelating agent, and can function as an antioxidant and anti-inflammatory agent. However, mangiferin has a low bioavailability. One of the methods to increase the bioavailability of mangiferin is to make mangiferin in the formulation of chitosan nanoparticles. This study aimed to determine the effect of mangiferin and mangiferin in chitosan nanoparticles on histopathology of rats liver given iron overload.

Methods: Thirty male Sprague-Dawley rats were divided into 5 groups: control (N), rats given iron overload (IO), IO + mangiferin dose of 50 mg/kg/day (M50), IO + mangiferin in chitosan nanoparticles dose of 25 mg/kg/day (MN25) and 50 mg/kg/day (MN50). After treatment, the rats were sacrificed and the liver was taken to make preparations. Observations under the microscope were carried out using visual field tests. The parameters studied were features of necrosis, inflammation, hyperplasia, and steatosis of the liver.

Results: The data retrieval process is still ongoing. It is estimated that iron overload given to rats will cause necrosis of the liver lobules, infiltration of inflammatory cells in the form of histiocytes and lymphocytes, Kupffer cell hyperplasia, and hepatic steatosis. The M50 treatment group is expected to provide a decrease in liver damage which is almost the same as MN25, whereas MN50 shows significant results in decreasing liver damage due to iron overload.

Conclusion: Mangiferin in chitosan nanoparticles can increase the bioavailability of mangiferin and is expected to reduce damage to the liver due to iron overload.

Keywords: mangiferin, chitosan-alginal nanoparticle, iron overload, liver, necrosis, hyperplasia, inflammation