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Integrating systematic pharmacology-based strategy and experimental validation to explore mechanism of Tripterygium glycoside on cholangiocyte-related liver injury

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Chinese Herbal Medicines 2022年第4期14卷 563-575页

作者： Yajing Li Sen Li Xiaoyong Xue Ting Wang Xiaojiaoyang Li School of Life Sciences Beijing University of Chinese MedicineBeijing 100029China Beijing Research Institute of Chinese Medicine Beijing University of Chinese MedicineBeijing 100029China

Objective:Tripterygium glycoside(TG)is widely used in clinical practice for its multiple bioactivities including anti-inflammatory and immunosuppressive ***,emerging studies have frequently reported TG-induced adverse reactions to multiple organs,especially ***,this study aimed to investigate the mechanism of liver damage induced by TG and explore representative components to reflect TG ***:Network pharmacology was used to determine the potential targets of bile duct injury caused by ***,the hepatotoxic effects of TG,triptolide(TP)and celastrol(CEL)were investigated and compared in vivo and in *** function was determined by measuring serum transaminase and histopathology *** cell proliferation and apoptosis were determined by cell viability assay,scratch assay and flow *** expression of gene of interest was determined by qPCR and Western ***:Based on the network pharmacological analysis of 12 bioactive ingredients found in TG,a total of35 targets and 15 pathways related to bile duct injury were *** TG and TP resulted in cholangiocyte damage and liver injury,as illustrated by increased levels of serum transaminase and oxidative stress,stimulated portal edema and lymphocytic infiltration and decreased expression of cholangiocyte marker,cytoskeletal *** addition,TG and TP inhibited cell proliferation and migration,arrested cell cycle and promoted Caspase-dependent apoptosis of cholangiocytes via suppressing the phosphorylation of extracellular regulated protein kinases 1/2(ERK1/2)and protein kinase B(AKT).While,CEL at equivalent dosage had no obvious ***:We revealed that TG-stimulated liver injury was specifically characterized by cholangiocyte damage and TP might be the decisive ingredient to reflect TG *** results not only provide novel insights into the mechanism underlying the hepatotoxicity effects of TG but also offer reference for clinic

关键词： cell apoptosis cholangiocyte liver injury Tripterygium glycoside triptolide

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Danhongqing formula alleviates cholestatic liver fibrosis by downregulating long non-coding RNA H19 derived from cholangiocytes and inhibiting hepatic stellate cell activation

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Journal of Integrative Medicine 2024年第2期22卷 188-198页

作者： Meng Li Yang Zhou Hui Zhu Lie-ming Xu Jian Ping Institute of Liver Diseases Shuguang HospitalShanghai University of Traditional Chinese MedicineShanghai 201203China Preventive Treatment Center Yueyang Hospital of Integrated Traditional Chinese and Western MedicineShanghai University of Traditional Chinese MedicineShanghai 200437 China Department of Gastroenterology Suzhou Traditional Chinese Medicine HospitalSuzhou 215000Jiangsu ProvinceChina Shanghai Key Laboratory of Traditional Chinese Medicine Shanghai 201203China Key Laboratory of Liver and Kidney Diseases(Ministry of Education) Shanghai 201203China

Objective:This study explores the mechanism of action of Danhongqing formula(DHQ),a compoundbased Chinese medicine formula,in the treatment of cholestatic liver ***:In vivo experiments were conducted using 8-week-old multidrug resistance protein 2 knockout(Mdr2-/-)mice as an animal model of cholestatic liver *** was administered orally for 8 weeks,and its impact on cholestatic liver fibrosis was evaluated by assessing liver function,liver histopathology,and the expression of liver fibrosis-related ***-time polymerase chain reaction,Western blot,immunohistochemistry and other methods were used to observe the effects of DHQ on long non-coding RNA H19(H19)and signal transducer and activator of transcription 3(STAT3)phosphorylation in the liver tissue of Mdr2-/-*** addition,cholangiocytes and hepatic stellate cells(HSCs)were cultured in vitro to measure the effects of bile acids on cholangiocyte injury and H19 *** overexpressing H19 were constructed,and a conditioned medium containing H19 was collected to measure its effects on STAT3 protein expression and cell *** intervention effect of DHQ on these processes was also *** overexpressing H19 were constructed to measure the impact of H19 on cell activation and assess the intervention effect of ***:DHQ alleviated liver injury,ductular reaction,and fibrosis in Mdr2-/-mice,and inhibited H19expression,STAT3 expression and STAT3 *** formula also reduced hydrophobic bile acid-induced cholangiocyte injury and the upregulation of H19,inhibited the activation of HSCs induced by cholangiocyte-derived conditioned medium,and decreased the expression of activation markers in *** overexpression of H19 in a human HSC line confirmed that H19 promoted STAT3 phosphorylation and HSC activation,and DHQ was able to successfully inhibit these ***:DHQ effectively alleviated spontaneous cholestatic liver fibrosis in Md

关键词： Liver cirrhosis biliary Long non-coding RNA H19 Danhongqing formula cholangiocyte Hepatic stellate cells STAT3 transcription factor

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Generation and metabolomic characterization of functional ductal organoids with biliary tree networks in decellularized liver scaffolds

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Bioactive Materials 2023年第8期26卷 452-464页

作者： Jiaxian Chen Shiwen Ma Hui Yang Xi Liang Heng Yao Beibei Guo Deying Chen Jing Jiang Dongyan Shi Jiaojiao Xin Keke Ren Xingping Zhou Yun Li Lei Geng Jun Li State Key Laboratory for Diagnosis and Treatment of Infectious Diseases National Clinical Research Center for Infectious DiseasesNational Medical Center for Infectious DiseasesCollaborative Innovation Center for Diagnosis and Treatment of Infectious DiseasesThe First Affiliated HospitalZhejiang University School of Medicine79 Qingchun Rd.Hangzhou310003China Precision Medicine Center Taizhou Central Hospital(Taizhou University Hospital)Taizhou318000China Institute of Pharmaceutical Biotechnology Zhejiang University School of MedicineHangzhou310013China Division of Hepatobiliary and Pancreatic Surgery Department of SurgeryThe First Affiliated HospitalZhejiang University School of Medicine79 Qingchun Rd.Hangzhou310003China

Developing functional ductal organoids(FDOs)is essential for liver regenerative *** aimed to construct FDOs with biliary tree networks in rat decellularized liver scaffolds(DLSs)with primary cholangiocytes isolated from mouse bile *** developed FDOs were dynamically characterized by functional assays and metabolomics for bioprocess *** were reconstructed in DLSs retaining native structure and bioactive factors with mouse primary cholangiocytes expressing enriched *** assessment showed that biliary tree-like structures gradually formed from day 3 to day *** cholangiocytes in FDOs maintained high viability and expressed 11 specific ***-apical polarity was observed at day 14 with immunostaining for E-cadherin and acetylatedα-*** rhodamine 123 transport assay and active collection of cholyl-lysyl-fluorescein exhibited the specific functions of bile secretion and transportation at day 14 compared to those in monolayer and hydrogel culture *** metabolomics analysis with 1075 peak pairs showed that serotonin,as a key molecule of the tryptophan metabolism pathway linked to biliary tree reconstruction,was specifically expressed in FDOs during the whole period of *** FDOs with biliary tree networks and serotonin expression may be applied for disease modeling and drug screening,which paves the way for future clinical therapeutic applications.

关键词： cholangiocyte Decellularized scaffold Ductal organoid Extracellular matrix

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Sequence of events leading to primary biliary cholangitis

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世界胃肠病学杂志:英文版 2023年第37期29卷 5305-5312页

作者： Ilaria Lenci Paola Carnì Martina Milana Agreta Bicaj Alessandro Signorello Leonardo Baiocchi Hepatology Unit University of Tor VergataRome 00133Italy Postgraduate School in Hepato/Gastroenterology Catholic University Our Lady of Good CounselTirana 1004Albania

Primary biliary cholangitis(PBC)is a chronic cholestatic liver disease that is observed more frequently in middle-aged *** disorder is considered an autoimmune disease,since liver injury is sustained by the presence of selfdirected antimitochondrial antibodies targeting the bile duct *** prognosis may vary depending on an early diagnosis and response to ***,nearly a third of patients can progress to liver cirrhosis,thus requiring a liver *** immunosuppressive therapies,commonly employed for other autoimmune diseases,have limited effects on *** fact,dramatic functional changes that occur in the biliary epithelium in the course of inflammation play a major role in perpetuating the *** this minireview,after a background on the disease and possible predisposing factors,the sequential cooperation of cellular/molecular events leading to end-stage PBC is discussed in *** rise and maintenance of the autoimmune process,as well as the response of the biliary epithelia during inflammatory injury,are key factors in the progression of the *** so-called“ductular reaction(DR)”,intended as a reactive expansion of cells with biliary phenotype,is a process frequently observed in PBC and partially ***,recent findings suggest a strict relationship between this pathological picture and the progression to liver fibrosis,cell senescence,and loss of biliary *** these issues(onset of chronic inflammation,changes in secretive and proliferative biliary functions,DR,and its relationship with other pathological events)are discussed in this manuscript in an attempt to provide a snapshot,for clinicians and researchers,of the most relevant and sequential contributors to the progression of this human cholestatic *** believe that interpreting this disorder as a multistep process may help identify possible therapeutic targets to prevent evolution to severe disease.

关键词： Primary biliary cholangitis cholangiocyte Biliary secretion Biliary proliferation Ductular reaction Antimitochondrial antibody Cellular senescence Liver fibrosis

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Hepatic senescence, the good and the bad

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World Journal of Gastroenterology 2019年第34期25卷 5069-5081页

作者： Nazmul Huda Gang Liu Honghai Hong Shengmin Yan Bilon Khambu Xiao-Ming Yin Department of Pathology and Laboratory Medicine Indiana University School of MedicineIndianapolis

Gradual alterations of cell’s physiology and functions due to age or exposure to various stresses lead to the conversion of normal cells to senescent *** becoming senescent,the cell stops dividing permanently but remains metabolically *** senescence does not have a single marker but is characterized mainly by a combination of multiple markers,such as,morphological changes,expression of cell cycle inhibitors,senescence associatedβ-galactosidase activity,and changes in nuclear *** cells in an organ become senescent,the entire organism can be *** may occur through the senescence-associated secretory phenotype(SASP).SASP may exert beneficial or harmful effects on the microenvironment of *** on senescence has become a very exciting field in cell biology since the link between age-related diseases,including cancer,and senescence has been *** loss of regenerative and homeostatic capacity of the liver over the age is somehow connected to cellular *** major contributors of senescence properties in the liver are hepatocytes and *** cells in the liver have been implicated in the etiology of chronic liver diseases including cirrhosis and hepatocellular carcinoma and in the interference of liver *** review summarizes recently reported findings in the understanding of the molecular mechanisms of senescence and its relationship with liver diseases.

关键词： Senescence Senescence associated secretory phenotype Hepatocyte cholangiocyte Hepatic stellate cell Cell cycle arrest DNA damage

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Somatic second-hit mutations leads to polycystic liver diseases

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World Journal of Gastroenterology 2013年第1期19卷 141-143页

作者： Jesús M Banales Patricia Munoz-Garrido Luis Bujanda Division of Hepatology and Gastroenterology Donostia Universitary HospitalBiodonostia Research InstituteE-20014 San SebastiánSpain Department of Liver and Gastrointestinal Diseases National Institute for the Study of Liver and Gastrointestinal Diseases(CIBERehdfunded by the Spanish Carlos III Institute)08036 BarcelonaSpain Ikerbasque Basque Foundation for Science48011 BilbaoSpain Spanish Association Against Cancer(AECC) 28040 MadridSpain

Polycystic liver diseases(PCLDs) are a heterogeneous group of genetic disorders characterized by the development of multiple fluid-filled cysts in the liver,which derive from cholangiocytes,the epithelial cells lining the bile *** these cysts grow,symptoms such as abdominal distension,nausea,and abdominal pain may *** may exist isolated(i.e.,autosomal dominant polycystic liver disease,ADPLD) or in combination with renal cystogenesis(i.e.,autosomal dominant polycystic kidney disease and autosomal recessive polycystic liver disease).The exact prevalence of PCLDs is unknown,but is estimated to occur in approximately 1:1000 *** the pathogenesis of each form of PCLD appears to be different,increasing evidences indicate that hepatic cystogenesis is a phenomenon that may involve somatic loss of heterozygosity(LOH) in those pathological conditions inherited in a dominant form.A recent report,using highly sophisticated methodology,demonstrated that ADPLD patients with a germline mutation in the protein kinase C substrate 80K-H(PRKCSH) gene mostly develop hepatic cystogenesis through a second somatic *** hepatocystin,the PRKCSH-encoding protein,was absent in the hepatic cysts with LOH,it was still expressed in the heterozygous *** the other hand,no additional trans-heterozygous mutations on the SEC63 homolog(*** /SEC63) gene(also involved in the development of PCLDs) were *** data indicate that PCLD is recessive at the cellular level,and point out the important role of hepatocystin loss in *** this commentary,we discuss the knowledge regarding the role of somatic second-hit mutations in the development of PCLDs,and the most relevant findings have been highlighted.

关键词： Polycystic liver diseases cholangiocyte Cystogenesis Loss of heterozygosity Protein kinase C substrate 80K-H SEC63

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