Corallodiscus flabellata B. L. Burtt extract alleviates lipopolysaccharide/D-galactosamine-induced acute liver failure and brain injury by inhibiting oxidative stress, apoptosis, and inflammation

Document Type: Original Article

Authors

1 College of Medicine, Henan University of Chinese Medicine, Zhengzhou 450046, China

2 The Engineering and Technology Center for Chinese Medicine Development of Henan Province, Zhengzhou 450046, China

10.22038/ijbms.2020.45437.10567

Abstract

Objective(s): Corallodiscus flabellata B. L. Burtt (CF) is distributed along liver meridian, with a possible beneficial effect in the progression of acute liver failure. Therefore, the present study investigates the effect of CF extract on rats with acute liver failure.
Materials and Methods: Rats were divided into four experimental groups: Control, Lipopolysaccharide (LPS)/D-Galactosamine (D-GalN) (L/D), Wu Ling Powder + L/D (WLP+L/D) and CF + L/D. Animals were gavage for 7 days, after which all animals except the control group were injected intraperitoneally with LPS and D-GalN to induce acute liver failure. Subsequently, the urine was collected for the next 8 hr, and the liver pathological changes were observed. The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), inflammatory factor and oxidative stress-related indicators were measured. The levels of reactive oxygen species (ROS), apoptosis marker in the liver, water content and aquaporin (AQPs) in the brain were detected. The concentration of ions and osmolality of urine and serum were determined.
Results: The results show that CF significantly improved the damage of liver and brain tissue, and reversed the changes of serum ALT, AST, inflammatory factor and Cl-. It modulated oxidative stress-related indicators, reduced the content of ROS, apoptosis markers, water content, the level of Cl- ions and osmolality in the urine and the expression of AQP1, and AQP4 in the brain, and increased the urine output.
Conclusion: It was found that the CF extract could alleviate the L/D induced acute liver failure by regulating the hepatocyte apoptosis and AQPs expression in the brain.

Keywords


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