2021
DOI: 10.3389/fphar.2020.597772
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Corrigendum: Inflammatory Stress Potentiates Emodin-Induced Liver Injury in Rats

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Cited by 3 publications
(2 citation statements)
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“…The liver plays a vital role in pathogen clearance and immunological reactions [ 102 ] and is susceptible to toxic chemical compounds, causing acute liver injury (ALI) [ 46 ]. Persistent liver damage can result in fibrosis and dysfunction [ 103 ], partly caused by lipopolysaccharide (LPS). LPS can induce liver injury [ 104 ] and activate receptors such as TLR4 in hepatocytes and Kupffer cells [ 105 ].…”
Section: Resultsmentioning
confidence: 99%
“…The liver plays a vital role in pathogen clearance and immunological reactions [ 102 ] and is susceptible to toxic chemical compounds, causing acute liver injury (ALI) [ 46 ]. Persistent liver damage can result in fibrosis and dysfunction [ 103 ], partly caused by lipopolysaccharide (LPS). LPS can induce liver injury [ 104 ] and activate receptors such as TLR4 in hepatocytes and Kupffer cells [ 105 ].…”
Section: Resultsmentioning
confidence: 99%
“…Two recent studies have shown that stilbene glycoside, one of the main components of RPM, can hinder emodin metabolism in the liver, expose emodin for a long time, affect bile acid metabolism, and promote emodin to cause obvious hepatotoxicity [ 42 , 43 ]. The use of emodin or stilbene glycoside alone had no significant effect [ 44 ]. It was reported that after RPM was processed, the content of emodin increased and the content of stilbene glycosides decreased, while stilbene glycosides were unstable under acidic conditions and easily degraded into stilbene aglycone at room temperature and further decomposed into phenols [ 45 ].…”
Section: Discussionmentioning
confidence: 99%