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Abstract Title:

The effects of astaxanthin on liver histopathology and expression of superoxide dismutase in rat aflatoxicosis.

Abstract Source:

J Vet Med Sci. 2019 Jul 3. Epub 2019 Jul 3. PMID: 31270307

Abstract Author(s):

Poempool Monmeesil, Wirasak Fungfuang, Phitsanu Tulayakul, Urai Pongchairerk

Article Affiliation:

Poempool Monmeesil

Abstract:

The metabolism of aflatoxin B(AFB) 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 AFB-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 AFBgroups were gavaged by water for 7 days followed by a single DMSO and 1 mg/kg AFB, respectively. The AXL+ AFBand AXH+ AFBgroups were given of 5 mg/kg and 100 mg/kg AX for 7 days before 1 mg/kg AFBadministration. The result showed significantly elevated liver weight per 100 g body weight in AFBgroup. The histopathological finding revealed vacuolar degeneration, necrosis, megalocytosis and binucleation of hepatocytes with bile duct hyperplasia in AFBgroup. The severities of pathological changes were sequentially reduced in AXL+AFBand AXH+AFBgroups. Most rats in AXH+AFBgroup 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+AFBgroup than solely treated AFBand AXL+AFBgroups. In conclusion, AX alleviated AFB-induced liver damage in rat by stimulating SOD1 expression and transdifferentiation of cholangiocytes in dose dependent manner.

Study Type : Animal Study

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