Effect of dihydromyricetin on hepatic encephalopathy associated with acute hepatic failure in mice

Abstract

Context

Hepatic encephalopathy (HE) is a complex neuropsychiatric disease caused by liver failure. Dihydromyricetin (DMY) is a traditional medicine used to treat liver injury.

Objective

To investigate the effects of dihydromyricetin (DMY) on hepatic encephalopathy associated with acute hepatic failure mice models established by thioacetamide (TAA) exposure.

Materials and methods

Female BALB/c mouse were randomly divided into control, DMY, TAA, and TAA + DMY groups (n = 8). The first two groups were intraperitoneally injected with saline or 5 mg/kg DMY, respectively. The last two groups were injected with 600 mg/kg TAA to establish HE models, and then the mice in the last group were treated with 5 mg/kg DMY. Neurological and cognition functions were evaluated 24 and 48 h after injection. Mice were sacrificed after which livers and brains were obtained for immunoblot and histopathological analysis, while blood was collected for the analysis of liver enzymes.

Results

In the TAA + DMY group, ALT and AST decreased to 145.31 ± 12.88 U/L and 309.51 ± 25.92 U/L, respectively, whereas ammonia and TBIL decreased to 415.67 ± 41.91 μmol/L and 3.31 ± 0.35 μmol/L, respectively. Moreover, MDA decreased to 10.74 ± 3.97 nmol/g, while SOD and GST increased to 398.69 ± 231.30 U/g and 41.37 ± 21.84 U/g, respectively. The neurological score decreased to 2.87 ± 0.63, and the number of GFAP-positive cells decreased to 41.10 ± 1.66. Furthermore, the protein levels of TNF-α, IL-6, and GABA_A in the cortex decreased.

Conclusions

We speculate that DMY can serve as a novel treatment for HE.

Keywords:

• Thioacetamide
• cognition functions
• liver enzymes
• glial fibrillary acidic protein
• GABAA receptor

Acknowledgement

The authors thank for the support of Key Laboratory of Digestive Diseases, Second Hospital of Lanzhou University.

Disclosure statement

The authors declare that there is no conflict of interest.

Additional information

Funding

This study was supported by the National Natural Science Foundation of China (No. 81770525) and Natural Science Foundation of Gansu Province (No. 17JR2JA191, 1506RJZA204 and 20JR5RA339).