The metabolism of aflatoxin B₁ (AFB₁) generates reactive oxygen species (ROS) that destroys hepatocytes. Meanwhile, astaxanthin (AX) is known to have stronger antioxidative activity than other carotenoids. This study aimed to investigate hepatoprotective role of AX from AFB₁-induced toxicity in rat by histopathological study and immunohistochemistry of Cu/Zn-SOD (SOD1) which acts as the first enzyme in antioxidative reaction against cell injury from ROS. Twenty Wistar rats were randomly divided into 4 groups. The control and AFB₁ groups were gavaged by water for 7 days followed by a single DMSO and 1 mg/kg AFB₁, respectively. The AXL+ AFB₁ and AXH+ AFB₁ groups were given of 5 mg/kg and 100 mg/kg AX for 7 days before 1 mg/kg AFB₁ administration. The result showed significantly elevated liver weight per 100 g body weight in AFB₁ group. The histopathological finding revealed vacuolar degeneration, necrosis, megalocytosis and binucleation of hepatocytes with bile duct hyperplasia in AFB₁ group. The severities of pathological changes were sequentially reduced in AXL+AFB₁ and AXH+AFB₁ groups. Most rats in AXH+AFB₁ group owned hypertrophic hepatocytes and atypical proliferation of cholangiocytes which are adaptive responses to severe hepatocyte damage. The SOD1 expression was also significantly higher in AXH+AFB₁ group than solely treated AFB₁ and AXL+AFB₁ groups. In conclusion, AX alleviated AFB₁-induced liver damage in rat by stimulating SOD1 expression and transdifferentiation of cholangiocytes in dose dependent manner.

Poempool MONMEESIL

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