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

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 failu...

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Main Authors: Long Cheng, Xiaoying Wang, Xueni Ma, Huimei Xu, Yifan Yang, Dekui Zhang
Format: Article
Language:English
Published: Taylor & Francis Group 2021-01-01
Series:Pharmaceutical Biology
Subjects:
Online Access:http://dx.doi.org/10.1080/13880209.2021.1917625
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author Long Cheng
Xiaoying Wang
Xueni Ma
Huimei Xu
Yifan Yang
Dekui Zhang
author_facet Long Cheng
Xiaoying Wang
Xueni Ma
Huimei Xu
Yifan Yang
Dekui Zhang
author_sort Long Cheng
collection DOAJ
description 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 GABAA in the cortex decreased. Conclusions We speculate that DMY can serve as a novel treatment for HE.
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spelling doaj.art-ecb6220af38e4e4da0a7477fe68822de2022-12-21T18:44:06ZengTaylor & Francis GroupPharmaceutical Biology1388-02091744-51162021-01-0159155756410.1080/13880209.2021.19176251917625Effect of dihydromyricetin on hepatic encephalopathy associated with acute hepatic failure in miceLong Cheng0Xiaoying Wang1Xueni Ma2Huimei Xu3Yifan Yang4Dekui Zhang5Department of Gastroenterology, Lanzhou University Second HospitalDepartment of Gastroenterology, Lanzhou University Second HospitalDepartment of Gastroenterology, Lanzhou University Second HospitalDepartment of Gastroenterology, Lanzhou University Second HospitalDepartment of Gastroenterology, Lanzhou University Second HospitalDepartment of Gastroenterology, Lanzhou University Second HospitalContext 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 GABAA in the cortex decreased. Conclusions We speculate that DMY can serve as a novel treatment for HE.http://dx.doi.org/10.1080/13880209.2021.1917625thioacetamidecognition functionsliver enzymesglial fibrillary acidic proteingabaa receptor
spellingShingle Long Cheng
Xiaoying Wang
Xueni Ma
Huimei Xu
Yifan Yang
Dekui Zhang
Effect of dihydromyricetin on hepatic encephalopathy associated with acute hepatic failure in mice
Pharmaceutical Biology
thioacetamide
cognition functions
liver enzymes
glial fibrillary acidic protein
gabaa receptor
title Effect of dihydromyricetin on hepatic encephalopathy associated with acute hepatic failure in mice
title_full Effect of dihydromyricetin on hepatic encephalopathy associated with acute hepatic failure in mice
title_fullStr Effect of dihydromyricetin on hepatic encephalopathy associated with acute hepatic failure in mice
title_full_unstemmed Effect of dihydromyricetin on hepatic encephalopathy associated with acute hepatic failure in mice
title_short Effect of dihydromyricetin on hepatic encephalopathy associated with acute hepatic failure in mice
title_sort effect of dihydromyricetin on hepatic encephalopathy associated with acute hepatic failure in mice
topic thioacetamide
cognition functions
liver enzymes
glial fibrillary acidic protein
gabaa receptor
url http://dx.doi.org/10.1080/13880209.2021.1917625
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