Berberine attenuate staphylococcal enterotoxin B-mediated acute liver injury via regulating HDAC expression
Abstract Staphylococcal enterotoxin B (SEB) has been documented to be implicated in the pathogenesis of liver injury in the experimental models of hepatitis. However, the underlying mechanism of SEB-induced acute liver injury (ALI) remains to be further explored. In our study, we explored the therap...
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doaj-4935cf6526d547828dfa2a33ded00ea22020-11-25T02:02:56ZengSpringerOpenAMB Express2191-08552018-10-018111010.1186/s13568-018-0684-2Berberine attenuate staphylococcal enterotoxin B-mediated acute liver injury via regulating HDAC expressionJiying Du0Xiaohua Ding1Xiaoqin Zhang2Xinyu Zhao3Huidong Shan4Fanping Wang5Institute of Inspection and Imaging, Sanquan Medical College, Xinxiang Medical UniversityInstitute of Inspection and Imaging, Sanquan Medical College, Xinxiang Medical UniversitySchool of Medical Examination, Xinxiang Medical UniversityInstitute of Inspection and Imaging, Sanquan Medical College, Xinxiang Medical UniversityInstitute of Inspection and Imaging, Sanquan Medical College, Xinxiang Medical UniversityBlood Immunology, School of Medical Examination, Xinxiang Medical UniversityAbstract Staphylococcal enterotoxin B (SEB) has been documented to be implicated in the pathogenesis of liver injury in the experimental models of hepatitis. However, the underlying mechanism of SEB-induced acute liver injury (ALI) remains to be further explored. In our study, we explored the therapeutic effectiveness of berberine (BBR), a natural isoquinoline alkaloid, in the SEB-induced ALI. In our study, we found that injection of SEB into d-galactosamine (d-gal)-sensitized mice induced ALI, as demonstrated by an increase of levels of alanine aminotransferase and aspartate aminotransferase, massive infiltration of immune cells into the liver, and pro-inflammatory cytokine release. However, intragastric administration of BBR attenuated SEB-induced ALI in mice. Meanwhile, we discovered that BBR treatment suppressed activation of splenocytes and pro-inflammatory cytokine release in SEB-stimulated splenocytes. Moreover, mechanistic analyses demonstrated that BBR was effective at inhibiting the expression of class I HDAC, but not class II, in SEB-stimulated splenocytes. Furthermore, trichostatin A, a standard HDAC inhibitor, alleviated activation of splenocytes and pro-inflammatory cytokine release in SEB-stimulated splenocytes. Taken together, we inferred from these results that BBR attenuated SEB-mediated ALI through repressing the class I HDAC enzyme, suggesting that BBR may constitute a novel therapeutic modality to prevent SEB-mediated inflammation and ALI.http://link.springer.com/article/10.1186/s13568-018-0684-2BBRSEBHDACSplenocytesAcute liver injury |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Jiying Du Xiaohua Ding Xiaoqin Zhang Xinyu Zhao Huidong Shan Fanping Wang |
spellingShingle |
Jiying Du Xiaohua Ding Xiaoqin Zhang Xinyu Zhao Huidong Shan Fanping Wang Berberine attenuate staphylococcal enterotoxin B-mediated acute liver injury via regulating HDAC expression AMB Express BBR SEB HDAC Splenocytes Acute liver injury |
author_facet |
Jiying Du Xiaohua Ding Xiaoqin Zhang Xinyu Zhao Huidong Shan Fanping Wang |
author_sort |
Jiying Du |
title |
Berberine attenuate staphylococcal enterotoxin B-mediated acute liver injury via regulating HDAC expression |
title_short |
Berberine attenuate staphylococcal enterotoxin B-mediated acute liver injury via regulating HDAC expression |
title_full |
Berberine attenuate staphylococcal enterotoxin B-mediated acute liver injury via regulating HDAC expression |
title_fullStr |
Berberine attenuate staphylococcal enterotoxin B-mediated acute liver injury via regulating HDAC expression |
title_full_unstemmed |
Berberine attenuate staphylococcal enterotoxin B-mediated acute liver injury via regulating HDAC expression |
title_sort |
berberine attenuate staphylococcal enterotoxin b-mediated acute liver injury via regulating hdac expression |
publisher |
SpringerOpen |
series |
AMB Express |
issn |
2191-0855 |
publishDate |
2018-10-01 |
description |
Abstract Staphylococcal enterotoxin B (SEB) has been documented to be implicated in the pathogenesis of liver injury in the experimental models of hepatitis. However, the underlying mechanism of SEB-induced acute liver injury (ALI) remains to be further explored. In our study, we explored the therapeutic effectiveness of berberine (BBR), a natural isoquinoline alkaloid, in the SEB-induced ALI. In our study, we found that injection of SEB into d-galactosamine (d-gal)-sensitized mice induced ALI, as demonstrated by an increase of levels of alanine aminotransferase and aspartate aminotransferase, massive infiltration of immune cells into the liver, and pro-inflammatory cytokine release. However, intragastric administration of BBR attenuated SEB-induced ALI in mice. Meanwhile, we discovered that BBR treatment suppressed activation of splenocytes and pro-inflammatory cytokine release in SEB-stimulated splenocytes. Moreover, mechanistic analyses demonstrated that BBR was effective at inhibiting the expression of class I HDAC, but not class II, in SEB-stimulated splenocytes. Furthermore, trichostatin A, a standard HDAC inhibitor, alleviated activation of splenocytes and pro-inflammatory cytokine release in SEB-stimulated splenocytes. Taken together, we inferred from these results that BBR attenuated SEB-mediated ALI through repressing the class I HDAC enzyme, suggesting that BBR may constitute a novel therapeutic modality to prevent SEB-mediated inflammation and ALI. |
topic |
BBR SEB HDAC Splenocytes Acute liver injury |
url |
http://link.springer.com/article/10.1186/s13568-018-0684-2 |
work_keys_str_mv |
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