Pediatric surgery international · 2026
Protective effects of astaxanthin on BDL-induced liver fibrosis: regulating MRP3 and AQP8 in cholestatic rats.
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Hashizume Naoki, Shin Ryusuke, Akiba Jun, Matsui Takanori, Sotogaku Naoki, Koga Yoshinori, Sotokawauchi Ami, Masui Daisuke, Sakamoto Saki, Sugita Koshiro, Yamagishi Sho-Ichi, Nishi Akinori, Kaji Tatsuru
Аннотация
PURPOSE: Liver fibrosis induced by cholestasis involves oxidative stress and activation of hepatic stellate cells. Astaxanthin (ASX), a potent antioxidant, may modulate this pathological process. This study aimed to evaluate the effect of ASX on cholestasis-induced fibrosis in a bile duct ligation (BDL) rat model.
METHODS: Male Wistar rats were randomly assigned to three groups: sham-operated, BDL with no treatment (NT), and BDL treated with ASX (100 mg/kg/day orally for 20 days). On day 21 post-surgery, liver and serum samples were collected. Biochemical assays, histological staining, immunohistochemistry, and quantitative PCR were performed to assess liver function, fibrosis, inflammation, and expression of aquaporins (AQP) and multidrug resistance-associated protein (MRP) transporters.
RESULTS: The ASX group showed significantly improved body weight gain and serum albumin compared to the NT group. While liver enzymes and bilirubin remained elevated, AQP8 expression was partially restored, and MRP3 was further upregulated by ASX. Although the degree of NF-κB staining grade and histological fibrosis grade in NT group was significantly higher than those in sham group, no significant differences were observed between sham group and ASX group.
CONCLUSION: The postoperative administration of ASX induced beneficial effects, resulting in the reduction of hepatic fibrosis via mechanisms involving the inhibition of NF-κB expression and improvement of AQP8 expression and enhancement of compensatory MRP3 activity.
METHODS: Male Wistar rats were randomly assigned to three groups: sham-operated, BDL with no treatment (NT), and BDL treated with ASX (100 mg/kg/day orally for 20 days). On day 21 post-surgery, liver and serum samples were collected. Biochemical assays, histological staining, immunohistochemistry, and quantitative PCR were performed to assess liver function, fibrosis, inflammation, and expression of aquaporins (AQP) and multidrug resistance-associated protein (MRP) transporters.
RESULTS: The ASX group showed significantly improved body weight gain and serum albumin compared to the NT group. While liver enzymes and bilirubin remained elevated, AQP8 expression was partially restored, and MRP3 was further upregulated by ASX. Although the degree of NF-κB staining grade and histological fibrosis grade in NT group was significantly higher than those in sham group, no significant differences were observed between sham group and ASX group.
CONCLUSION: The postoperative administration of ASX induced beneficial effects, resulting in the reduction of hepatic fibrosis via mechanisms involving the inhibition of NF-κB expression and improvement of AQP8 expression and enhancement of compensatory MRP3 activity.