Piceatannol Ameliorates Hepatic Oxidative Damage and Mitochondrial Dysfunction of Weaned Piglets Challenged with Diquat

Abstract

Simple Summary

In our experiment, piglets in two challenged groups were orally administrated either piceatannol or another vehicle solution, and then injected with diquat, a bipyridyl herbicide that can cause a large amount of reactive oxygen species in animal bodies and is widely used to cause oxidative stress, to investigate the effects of piceatannol on hepatic redox status, mitochondrial function and the underlying mechanism. A control group was given neither piceatannol supplementation nor diquat injection. Results showed that piceatannol could improve hepatic redox status, preserve mitochondrial function, and prevent excessive apoptosis of liver cells. In addition, piceatannol might exert its protective effects through a classic antioxidant signaling pathway named Nrf2. Our findings indicated that piceatannol might be an appropriate candidate for further development as an antioxidant food supplement to minimize the risk of oxidative stress in young animals.

Abstract

The liver is an organ that produces large amounts of reactive oxygen species (ROS). Human infants or piglets are prone to oxidative damage due to their uncompleted development of the antioxidant system, causing liver disease. Piceatannol (PIC) has been found to have significant antioxidant effects. The aim of this experiment was to investigate the effects of PIC on the liver in piglets experiencing oxidative stress caused by diquat (DQ). After weaning, 54 male piglets (Duroc × [Landrace × Yorkshire]) were selected and randomly divided into three treatment groups: the CON group, the DQ-CON group, and the DQ-PIC group. The two challenged groups were injected with DQ and then orally administrated either PIC or another vehicle solution, while the control group was given sterile saline injections and an orally administrated vehicle solution. Compared to the results of the CON group, DQ increased the percentage of apoptosis cells in the liver, also decreased the amount of reduced glutathione (GSH) and increased the concentration of malondialdehyde (MDA). In addition, the adenosine triphosphate (ATP) production, activities of mitochondrial complex I, II, III, and V, and the protein expression level of sirtuin 1 (SIRT1) were inhibited by DQ. Furthermore, PIC supplementation inhibited the apoptosis of hepatic cells caused by DQ. PIC also decreased MDA levels and increased the amount of GSH. Piglets given PIC supplementation exhibited increased activities of mitochondrial complex I, II, III, and V, the protein expression level of SIRT1, and the ATP production in the liver. In conclusion, PIC affected the liver of piglets by improving redox status, preserving mitochondrial function, and preventing excessive apoptosis.