Molecular biology reports · 2026
Rutin attenuates acrylamide-induced oxidative liver injury.
СтатьяНазвание и аннотация: Перевод в очереди
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Zhang Chunmei, Wang Shuai, Zhang Xiaoyun, Liu Yan, Chen Yixiang
Аннотация
BACKGROUND: Acrylamide (ACR) is an important chemical raw material, and its toxic effects have been confirmed in vitro and in vivo. However, only a few studies have investigated ACR-induced liver injury. As a naturally occurring flavonoid widely distributed across the plant kingdom, rutin (Rut) possesses notable pharmacological properties. This study aimed to demonstrate its therapeutic potential in mitigating ACR-induced hepatic injury in rats. Accordingly, an intervention model was established to explore the mechanistic basis of the protective effects of Rut against ACR-induced liver injury.
METHODS: The experimental design comprised five cohorts (n = 10), consisting of 50 male Sprague-Dawley rats randomly assigned to each group: (1) Control (0.5% CMC-Na + ddH2O), (2) ACR (20 mg/kg/day via gavage), (3) Rut-L (100 mg/kg) + ACR, (4) Rut-M (200 mg/kg) + ACR, and (5) Rut-H (400 mg/kg) + ACR. Interventions lasted for 21 days. The body weights of the animals were monitored daily. The liver coefficient (liver weight/body weight) was calculated after euthanasia. Commercial assay kits were used to determine serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities and hepatic Superoxide Dismutase (SOD), Glutathione (GSH), and Malondialdehyde (MDA) levels. Histopathological changes were assessed using Hematoxylin and eosin and Masson staining. Tumor Necrosis Factor-α (TNF-α) and cleaved caspase-3 expression levels were analyzed using immunohistochemistry.
RESULTS: Compared with the Control group, ACR exposure attenuated the rate of body weight accrual (P < 0.05) and the liver-to-body weight ratio (P < 0.05), elevated serum ALT (↑34.8%, P < 0.05) and AST (↑47.7%, P < 0.05), decreased hepatic SOD (↓48.9%, P < 0.05) and GSH (↓17.7%, P < 0.05), and increased MDA (↑38.8%, P < 0.05). High-dose Rut reversed these effects by increasing body weight gain (P < 0.01), liver coefficient (↑29.4%, P < 0.05), SOD (↑32.1%, P < 0.05), and GSH (↑12.1%, P < 0.05), while reducing ALT (↓22.9%, P < 0.01), AST (↓16.8%, P < 0.01), and MDA (↓9.0%, P < 0.05) levels. Histopathological analysis demonstrated reduced hepatocyte necrosis and collagen deposition in the Rut-treated group. Immunohistochemistry revealed that ACR increased TNF-α (↑121.4%, P < 0.001) and cleaved caspase-3 (↑97.8%, P < 0.001) expression, which was suppressed by Rut (TNF-α: ↓48.2%, P < 0.01; cleaved caspase-3: ↓39.5%, P < 0.01). The effect sizes (Cohen's d) ranged from 1.2 to 3.6, indicating robust effects.
CONCLUSION: Rut exhibits a marked protective effect against ACR-induced hepatic injury. Therefore, Rut may be considered a potential agent for preventing ACR-induced liver injury in rats.
METHODS: The experimental design comprised five cohorts (n = 10), consisting of 50 male Sprague-Dawley rats randomly assigned to each group: (1) Control (0.5% CMC-Na + ddH2O), (2) ACR (20 mg/kg/day via gavage), (3) Rut-L (100 mg/kg) + ACR, (4) Rut-M (200 mg/kg) + ACR, and (5) Rut-H (400 mg/kg) + ACR. Interventions lasted for 21 days. The body weights of the animals were monitored daily. The liver coefficient (liver weight/body weight) was calculated after euthanasia. Commercial assay kits were used to determine serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities and hepatic Superoxide Dismutase (SOD), Glutathione (GSH), and Malondialdehyde (MDA) levels. Histopathological changes were assessed using Hematoxylin and eosin and Masson staining. Tumor Necrosis Factor-α (TNF-α) and cleaved caspase-3 expression levels were analyzed using immunohistochemistry.
RESULTS: Compared with the Control group, ACR exposure attenuated the rate of body weight accrual (P < 0.05) and the liver-to-body weight ratio (P < 0.05), elevated serum ALT (↑34.8%, P < 0.05) and AST (↑47.7%, P < 0.05), decreased hepatic SOD (↓48.9%, P < 0.05) and GSH (↓17.7%, P < 0.05), and increased MDA (↑38.8%, P < 0.05). High-dose Rut reversed these effects by increasing body weight gain (P < 0.01), liver coefficient (↑29.4%, P < 0.05), SOD (↑32.1%, P < 0.05), and GSH (↑12.1%, P < 0.05), while reducing ALT (↓22.9%, P < 0.01), AST (↓16.8%, P < 0.01), and MDA (↓9.0%, P < 0.05) levels. Histopathological analysis demonstrated reduced hepatocyte necrosis and collagen deposition in the Rut-treated group. Immunohistochemistry revealed that ACR increased TNF-α (↑121.4%, P < 0.001) and cleaved caspase-3 (↑97.8%, P < 0.001) expression, which was suppressed by Rut (TNF-α: ↓48.2%, P < 0.01; cleaved caspase-3: ↓39.5%, P < 0.01). The effect sizes (Cohen's d) ranged from 1.2 to 3.6, indicating robust effects.
CONCLUSION: Rut exhibits a marked protective effect against ACR-induced hepatic injury. Therefore, Rut may be considered a potential agent for preventing ACR-induced liver injury in rats.