RETRACTED: Calycosin inhibits hepatocyte apoptosis in acute liver failure by suppressing the TLR4/NF‐κB pathway: An in vitro study
Abstract Background Acute liver failure (ALF) is a serious liver disease that is difficult to treat owing to its unclear pathogenesis. This study aimed to investigate the roles and molecular mechanisms of calycosin (CA) in ALF. Methods In this study, the roles and mechanism of CA in ALF were explore...
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| Format: | Article |
| Language: | English |
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Wiley
2023-07-01
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| Series: | Immunity, Inflammation and Disease |
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| Online Access: | https://doi.org/10.1002/iid3.935 |
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| author | Le Chang Aiqing Zhang Wenjuan Liu Ping Cao Lixian Dong Xiaoxue Gao |
| author_facet | Le Chang Aiqing Zhang Wenjuan Liu Ping Cao Lixian Dong Xiaoxue Gao |
| author_sort | Le Chang |
| collection | DOAJ |
| description | Abstract Background Acute liver failure (ALF) is a serious liver disease that is difficult to treat owing to its unclear pathogenesis. This study aimed to investigate the roles and molecular mechanisms of calycosin (CA) in ALF. Methods In this study, the roles and mechanism of CA in ALF were explored using an in vitro lipopolysaccharide (LPS)‐induced ALF cell model. Additionally, 3‐(4,5‐dimethyl‐2‐thiazolyl)−2,5‐diphenyltetrazolium bromide assay was used to assess the effect of CA on the activity of LPS‐induced L02 human liver epithelial cells, and flow cytometry was used to detect apoptosis in L02 cells. Expression levels of apoptosis‐related genes, Bax and Bcl‐2, were measured using reverse transcription‐quantitative polymerase chain reaction and Western blot analysis. Expression levels of inflammatory factors in LPS‐induced L02 cells were measured using an enzyme‐linked immunosorbent assay. Additionally, the effect of CA on ALF was inhibited via transfection of a toll‐like receptor 4 (TLR4)‐plasmid to elucidate the relationship between CA and TLR4/nuclear factor (NF)‐κB signaling pathway in ALF. Results CA had no toxic effects on L02 cells, but enhanced the activity of LPS‐induced L02 cells in a dose‐dependent manner. Apoptosis and inflammatory factor release was increased in ALF, activating the TLR4/NF‐κB signaling pathway. However, CA treatment inhibited the apoptosis and release of inflammatory factors. Further mechanistic studies revealed that the upregulation of TLR4 expression reversed the alleviating effects of CA on inflammation and apoptosis in LPS‐induced L02 cells. Conclusion CA alleviates inflammatory damage in LPS‐induced L02 cells by inhibiting the TLR4/NF‐κB pathway and may be a promising therapeutic agent for ALF treatment. |
| format | Article |
| id | doaj-art-e2f9b6c4d33741ebbf329f69dbf3adb4 |
| institution | Kabale University |
| issn | 2050-4527 |
| language | English |
| publishDate | 2023-07-01 |
| publisher | Wiley |
| record_format | Article |
| series | Immunity, Inflammation and Disease |
| spelling | doaj-art-e2f9b6c4d33741ebbf329f69dbf3adb42025-08-20T03:56:09ZengWileyImmunity, Inflammation and Disease2050-45272023-07-01117n/an/a10.1002/iid3.935RETRACTED: Calycosin inhibits hepatocyte apoptosis in acute liver failure by suppressing the TLR4/NF‐κB pathway: An in vitro studyLe Chang0Aiqing Zhang1Wenjuan Liu2Ping Cao3Lixian Dong4Xiaoxue Gao5Gastroenterology Department, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital Third Hospital of Shanxi Medical University Taiyuan ChinaGastroenterology Department, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital Third Hospital of Shanxi Medical University Taiyuan ChinaGastroenterology Department, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital Third Hospital of Shanxi Medical University Taiyuan ChinaGastroenterology Department, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital Third Hospital of Shanxi Medical University Taiyuan ChinaGastroenterology Department, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital Third Hospital of Shanxi Medical University Taiyuan ChinaGastroenterology Department, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital Third Hospital of Shanxi Medical University Taiyuan ChinaAbstract Background Acute liver failure (ALF) is a serious liver disease that is difficult to treat owing to its unclear pathogenesis. This study aimed to investigate the roles and molecular mechanisms of calycosin (CA) in ALF. Methods In this study, the roles and mechanism of CA in ALF were explored using an in vitro lipopolysaccharide (LPS)‐induced ALF cell model. Additionally, 3‐(4,5‐dimethyl‐2‐thiazolyl)−2,5‐diphenyltetrazolium bromide assay was used to assess the effect of CA on the activity of LPS‐induced L02 human liver epithelial cells, and flow cytometry was used to detect apoptosis in L02 cells. Expression levels of apoptosis‐related genes, Bax and Bcl‐2, were measured using reverse transcription‐quantitative polymerase chain reaction and Western blot analysis. Expression levels of inflammatory factors in LPS‐induced L02 cells were measured using an enzyme‐linked immunosorbent assay. Additionally, the effect of CA on ALF was inhibited via transfection of a toll‐like receptor 4 (TLR4)‐plasmid to elucidate the relationship between CA and TLR4/nuclear factor (NF)‐κB signaling pathway in ALF. Results CA had no toxic effects on L02 cells, but enhanced the activity of LPS‐induced L02 cells in a dose‐dependent manner. Apoptosis and inflammatory factor release was increased in ALF, activating the TLR4/NF‐κB signaling pathway. However, CA treatment inhibited the apoptosis and release of inflammatory factors. Further mechanistic studies revealed that the upregulation of TLR4 expression reversed the alleviating effects of CA on inflammation and apoptosis in LPS‐induced L02 cells. Conclusion CA alleviates inflammatory damage in LPS‐induced L02 cells by inhibiting the TLR4/NF‐κB pathway and may be a promising therapeutic agent for ALF treatment.https://doi.org/10.1002/iid3.935calycosinhepatocytes apoptosisinflammationlipopolysaccharideliver injury |
| spellingShingle | Le Chang Aiqing Zhang Wenjuan Liu Ping Cao Lixian Dong Xiaoxue Gao RETRACTED: Calycosin inhibits hepatocyte apoptosis in acute liver failure by suppressing the TLR4/NF‐κB pathway: An in vitro study Immunity, Inflammation and Disease calycosin hepatocytes apoptosis inflammation lipopolysaccharide liver injury |
| title | RETRACTED: Calycosin inhibits hepatocyte apoptosis in acute liver failure by suppressing the TLR4/NF‐κB pathway: An in vitro study |
| title_full | RETRACTED: Calycosin inhibits hepatocyte apoptosis in acute liver failure by suppressing the TLR4/NF‐κB pathway: An in vitro study |
| title_fullStr | RETRACTED: Calycosin inhibits hepatocyte apoptosis in acute liver failure by suppressing the TLR4/NF‐κB pathway: An in vitro study |
| title_full_unstemmed | RETRACTED: Calycosin inhibits hepatocyte apoptosis in acute liver failure by suppressing the TLR4/NF‐κB pathway: An in vitro study |
| title_short | RETRACTED: Calycosin inhibits hepatocyte apoptosis in acute liver failure by suppressing the TLR4/NF‐κB pathway: An in vitro study |
| title_sort | retracted calycosin inhibits hepatocyte apoptosis in acute liver failure by suppressing the tlr4 nf κb pathway an in vitro study |
| topic | calycosin hepatocytes apoptosis inflammation lipopolysaccharide liver injury |
| url | https://doi.org/10.1002/iid3.935 |
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