Molecular biology reports · 2026
Hepatoprotective effects of cinnamic acid against carbon tetrachloride-induced liver injury in a mouse model.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Nomiri Samira, Taebi Reyhaneh, Mohammadi Yaser, Yousefi Tooba, Asgari Fatemeh, Yazdanimoghaddam Farzaneh, Mortazavi Nafiseh, Amini Abdollah
Аннотация
BACKGROUND: Cinnamic acid (CA), a natural phenolic compound with antioxidant and anti-inflammatory properties, has recently attracted attention for its potential protective effects on liver function. This study aimed to evaluate the hepatoprotective effects of CA against carbon tetrachloride (CCl₄)-induced toxicity in mice.
METHODS: Thirty NMRI mice were randomly divided into five groups: control, CCl₄, and three groups treated with CA (50, 100, and 200 mg/kg). CA was administered orally for seven days prior to CCl₄ injection. Serum biochemical parameters and total antioxidant capacity (TAC) were measured. Gene expression levels of Nrf2, Foxo3, IL-6, and TNF-α, as well as liver histology, were also assessed.
RESULTS: CCl₄ exposure markedly elevated hepatic enzymes, bilirubin, urea, and C-reactive protein (CRP) levels while reducing albumin and total protein concentrations. Pretreatment with CA improved several of these parameters, particularly at higher doses (100-200 mg/kg). Although CA treatment did not significantly restore TAC levels, higher CA doses (100-200 mg/kg) upregulated Nrf2 and Foxo3, suggesting activation of antioxidant-related signaling pathways, and downregulated IL-6 and TNF-α expression, indicating reduced inflammatory marker expression. TNF-α. Histopathological analysis confirmed these biochemical findings, showing reduced necrosis and inflammation in CA-treated mice.
CONCLUSION: Cinnamic acid may exert hepatoprotective effects against CCl₄-induced liver injury, with secondary favorable effects on renal biochemical markers of CCl₄-induced systemic toxicity, by modulating oxidative and inflammatory pathways. Its association with increased Nrf2 and Foxo3 expression and reduced inflammatory mediator expression supports further investigation of CA as a potential hepatoprotective compound.
METHODS: Thirty NMRI mice were randomly divided into five groups: control, CCl₄, and three groups treated with CA (50, 100, and 200 mg/kg). CA was administered orally for seven days prior to CCl₄ injection. Serum biochemical parameters and total antioxidant capacity (TAC) were measured. Gene expression levels of Nrf2, Foxo3, IL-6, and TNF-α, as well as liver histology, were also assessed.
RESULTS: CCl₄ exposure markedly elevated hepatic enzymes, bilirubin, urea, and C-reactive protein (CRP) levels while reducing albumin and total protein concentrations. Pretreatment with CA improved several of these parameters, particularly at higher doses (100-200 mg/kg). Although CA treatment did not significantly restore TAC levels, higher CA doses (100-200 mg/kg) upregulated Nrf2 and Foxo3, suggesting activation of antioxidant-related signaling pathways, and downregulated IL-6 and TNF-α expression, indicating reduced inflammatory marker expression. TNF-α. Histopathological analysis confirmed these biochemical findings, showing reduced necrosis and inflammation in CA-treated mice.
CONCLUSION: Cinnamic acid may exert hepatoprotective effects against CCl₄-induced liver injury, with secondary favorable effects on renal biochemical markers of CCl₄-induced systemic toxicity, by modulating oxidative and inflammatory pathways. Its association with increased Nrf2 and Foxo3 expression and reduced inflammatory mediator expression supports further investigation of CA as a potential hepatoprotective compound.