지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2020.1
- 수록면
- 19 - 27 (9page)
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Background: Bile duct ligation (BDL) has been used for experimental research on hepatic encephalopathy (HE) caused by chronic liver disease. However, little research has been done on a BDL model in C57BL/6 mouse. Therefore, we evaluated the suitability of a BDL model in C57BL/6 mouse for the study of HE and determined which behavioral tests are appropriate for the identification of HE in this model. Methods: Twelve to fourteen-week-old male C57BL/6 mice were randomly assigned to either sham group or BDL group. Histological changes in liver were confirmed by hematoxylin/ eosin and Masson’s trichrome staining. Liver function alterations were detected by alanine aminotransferase (ALT) and ammonia levels. To identify behavioral changes, open field, elevated plus maze, novel object recognition, and passive avoidance tests were performed. Results: Inflammatory liver injury and fibrosis were observed 14 days after BDL. ALT and ammonia levels were significantly higher in BDL group than in sham group. There were no differences in general locomotor activity or anxiety between the groups. No difference was observed between these two groups in the novel object recognition test, but BDL group showed significant learning/memory impairment in the passive avoidance test compared to sham group. Conclusions: Fourteen days of BDL in 12–14-week-old male C57BL/6 mice is a clinically relevant model for HE, as these mice have liver fibrosis with impaired liver function, hyperammonemia, and learning/memory impairment. Passive avoidance can be used as the major behavioral test in this model of HE.
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참고문헌 (30)
참고문헌 신청
Vilstrup H / 2014 / Hepatic encephalopathy in chronic liver disease : 2014 Practice Guideline by the American Association for the Study of Liver Diseases and the European Association for the Study of the Liver / Hepatology 60:715~735
Basu PP / 2015 / Clinical and neurologic manifestation of minimal hepatic encephalopathy and overt hepatic encephalopathy / Clin Liver Dis 19:461~472
Butterworth RF / 2009 / Experimental models of hepatic encephalopathy : ISHEN guidelines / Liver Int 29:783~788
McMillin M / 2014 / Neuronal CCL2 is upregulated during hepatic encephalopathy and contributes to microglia activation and neurological decline / J Neuroinflammation 11:121
Chastre A / 2014 / Lipopolysaccharide precipitates hepatic encephalopathy and increases blood-brain barrier permeability in mice with acute liver failure / Liver Int 34:353~361
Basu PP / 2015 / Clinical and neurologic manifestation of minimal hepatic encephalopathy and overt hepatic encephalopathy / Clin Liver Dis 19:461~472
Butterworth RF / 2009 / Experimental models of hepatic encephalopathy : ISHEN guidelines / Liver Int 29:783~788
McMillin M / 2014 / Neuronal CCL2 is upregulated during hepatic encephalopathy and contributes to microglia activation and neurological decline / J Neuroinflammation 11:121
Chastre A / 2014 / Lipopolysaccharide precipitates hepatic encephalopathy and increases blood-brain barrier permeability in mice with acute liver failure / Liver Int 34:353~361
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