Abstract
Purpose: To investigate whether aloperine pretreatment ameliorates acute liver injury in carbon tetrachloride (CCl4)-treated mice.Methods: Mice were injected with CCl4 and orally administered aloperine. Blood samples and liver tissues were used for histopathological and biochemical analyses, respectively. Protein expression levels were determined by western blotting.Results: Histopathological analysis indicate that aloperine pretreatment significantly alleviated CCl4- induced mouse hepatic injury. CCl4 treatment induced the upregulation of aspartate aminotransferase (AST), alkaline phosphatase (ALP), alanine amino transferase (ALT), and total bilirubin (p < 0.05). However, these alterations were significantly inhibited by aloperine treatment. Moreover, aloperine pretreatment markedly decreased (p < 0.05) the CCl4-induced expression of oxidative stress biomarkers, including malondrialdeline (MDA), glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD). Compared to the control group, the protein levels of Nrf2, HO-1, iNOS, and COX-2 were significantly increased in the CCl4 group, while Nrf2 and HO-1 were upregulated. Furthermore, iNOS and COX-2 were downregulated in mouse liver in CCl4 + aloperine group compared to CCl4 group in a concentration-dependent manner (p < 0.05).Conclusion: Aloperine pretreatment appears to markedly upregulate Nrf2 and HO-1 and downregulate iNOS and COX-2 to suppress hepatic injury in mice. Thus, aloperine is a promising treatment for acute liver injury.
 Keywords: Hepatic injury, Aloperine, Oxidative stress, Nrf2/HO-1 pathway
Highlights
Environmental toxins often disturb hepatic metabolic function and increase the expression of liver enzymes, leading to liver fibrosis, cirrhosis, and even cancer [1]
The present study was undertaken to explore the influence of aloperine pretreatment on acute liver injury caused by CCl4 in mice and determine the possible involvement of the Nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway in this process
These findings demonstrate that aloperine reduces CCl4-induced liver damage in mice
Summary
Environmental toxins often disturb hepatic metabolic function and increase the expression of liver enzymes, leading to liver fibrosis, cirrhosis, and even cancer [1]. Carbon tetrachloride (CCl4) is frequently used to induce liver injury and to study the effects of chemical compounds on the liver [3]. Interventions that target the Nrf2/HO-1 signaling pathway have recently been suggested to be important therapeutic approaches for the treatment of alcoholic liver injury [7]. The combination of metformin and luteolin has been reported to reduce liver injury induced by CCl4 by activating the Nrf2/HO-1 pathway [9]. A recent study showed that aloperine protects mice from ischemia-reperfusion-induced renal injury by reducing levels of oxidative stress [12]. The present study was undertaken to explore the influence of aloperine pretreatment on acute liver injury caused by CCl4 in mice and determine the possible involvement of the Nrf2/HO-1 pathway in this process. Ten different views of an image were randomly chosen and scored by two pathologists independently
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