Alisol B 23-acetate promotes liver regeneration in mice after partial hepatectomy via activating farnesoid X receptor

Meng, Qiang; Chen, Han Y. H.; Wang, Changyuan; Liu, Qi; Sun, Huijun; Sun, Pengyuan; Peng, Jinyong; Liu, Kexin

doi:10.1016/j.bcp.2014.09.009

Cited by 34 publications

(21 citation statements)

References 36 publications

(38 reference statements)

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“…Most importantly, EE was proved to orchestrate adaptive response by activating FXR, indicating that as the key regulatory transcription factor for bile acid, FXR may become the focus of targeted therapies in cholestasis (34). We have shown that AB23A is an exogenous activator of FXR in the previous studies (15,16). In the present study, we used FXR antagonist GS in mice to verify that AB23A activate FXR to regulate expression level of genes in bile acid homeostasis.…”

Section: Discussionmentioning

confidence: 70%

“…Many pharmacological studies have revealed that AB23A has several pharmacological activities, such as antihepatitis virus, anti-proliferative activity of cancer cell lines and antibacterial effects (12)(13)(14). Recently, we have demonstrated that AB23A has promotive effect on liver regeneration and protective effect through FXR activation in mice (15,16). Therefore, an intriguing and important question arises whether AB23A has hepatoprotective effect on cholestatic liver injury such as EE-induced hepatic toxicity and cholestasis.…”

Section: Introductionmentioning

confidence: 96%

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Protective Effects of Alisol B 23-Acetate Via Farnesoid X Receptor-Mediated Regulation of Transporters and Enzymes in Estrogen-Induced Cholestatic Liver Injury in Mice

et al. 2015

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Section: Discussionmentioning

confidence: 70%

Section: Introductionmentioning

confidence: 96%

Protective Effects of Alisol B 23-Acetate Via Farnesoid X Receptor-Mediated Regulation of Transporters and Enzymes in Estrogen-Induced Cholestatic Liver Injury in Mice

et al. 2015

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“…34 Nevertheless, recent findings evidence a role of these pathways, or at least of some related proteins, in promoting cell regeneration both in normal and cancer tissues. [35][36][37] In addition, SERPINF1 (also known as PEDF) that is secreted by Muse cells and belong both to LXR/RXR and FXR/RXR pathways promotes selfrenewal a maintaining multipotency of several stem cell types. [38][39][40] Muse cells secrete factors that may regulate immune system functions The proteins belonging to i) Antigen presentation pathway; ii) Coagulation system; iii) FXR/RXR Activation and iiii) LXR/ RXR Activation pathways may play a role in immunomodulation (Fig.…”

Section: Muse Cells Secrete Factors That May Play a Role In Stem Cellmentioning

confidence: 99%

The secretome of MUSE cells contains factors that may play a role in regulation of stemness, apoptosis and immunomodulation

et al. 2016

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Mesenchymal stromal cells (MSCs) are a heterogeneous population, which contain several cell phenotypes: mesenchymal stem cells, progenitor cells, fibroblasts and other type of cells. Previously, we identified unique stem cells that we named multilineage-differentiating stress enduring (Muse) cells as one to several percent of MSCs of the bone marrow, adipose tissue and dermis. Among different cell populations in MSCs, Muse cells, positive for pluripotent surface marker SSEA-3, may represent cells responsible for pluripotent-like property of MSCs, since they express pluripotency genes, able to differentiated into triploblastic cells from a single cells and are self-renewable.MSCs release biologically active factors that have profound effects on local cellular dynamics. A thorough examination of MSC secretome seems essential for understanding the physiological functions exerted by these cells in our organism and also for rational cellular therapy design. In this setting, studies on secretome of Muse cells may shed light on pathways that are associated with their specific features.Our findings evidenced that secretomes of MSCs and Muse cells contain factors that regulate extracellular matrix remodeling, ox-redox activities and immune system. Muse cells appear to secrete factors that may preserve their stem cell features, allow survival under stress conditions and may contribute to their immunomodulation capacity.In detail, the proteins belonging to protein kinase A signaling, FXR/RXR activation and LXR/RXR activation pathways may play a role in regulation of Muse stem cell features. These last 2 pathways together with proteins associated with antigen presentation pathway and coagulation system may play a role in immunomodulation.

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“…Cholic acid feeding augmented liver regeneration following PHx in Fxr-dependent manner [26]. Dose-dependent stimulation of liver regeneration was also observed in mice given alisol B 23-acetate, a plant triterpenoid with FXR agonistic activity [58]. Lastly, the synthetic FXR agonist Px20350 could overcome defective regeneration in aged mice [39].…”

Section: Pharmacological Modulation Of Liver Regeneration By Bile Salmentioning

confidence: 93%

The role of bile salts in liver regeneration

et al. 2016

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A growing body of evidence has demonstrated that bile salts are important for liver regeneration following partial hepatectomy. The relative bile salt overload after partial liver resection causes activation of bile salt receptors in non-parenchymal (viz. the plasma membrane receptor TGR5) and parenchymal (viz. the intracellular receptor FXR) cells in the liver, thus, providing signals to the regenerative process. Impaired bile salt signaling in mice with genetic deficiency of Tgr5 or Fxr results in delayed liver regeneration after partial hepatectomy, and is accompanied by mortality in case of Fxr knock-out mice. Conversely, compensatory liver re-growth in hepatectomized mice can be stimulated by feeding of bile salts or alisol B 23-acetate, a natural triterpenoid agonist of Fxr. A large number of animal studies underscore the importance of strict maintenance of bile salt homeostasis for proper progression of liver regeneration. Both ileal and hepatic Fxr play a key role in regulation of bile salt homeostasis and, thus, preventing hepatotoxicity caused by excessive levels of bile salts. They further contribute to liver regeneration by induction of mitogenic factors. Agents that target bile salt receptors hold promise as drugs to stimulate liver regeneration in selected patients.

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Alisol B 23-acetate promotes liver regeneration in mice after partial hepatectomy via activating farnesoid X receptor

Cited by 34 publications

References 36 publications

Protective Effects of Alisol B 23-Acetate Via Farnesoid X Receptor-Mediated Regulation of Transporters and Enzymes in Estrogen-Induced Cholestatic Liver Injury in Mice

Protective Effects of Alisol B 23-Acetate Via Farnesoid X Receptor-Mediated Regulation of Transporters and Enzymes in Estrogen-Induced Cholestatic Liver Injury in Mice

The secretome of MUSE cells contains factors that may play a role in regulation of stemness, apoptosis and immunomodulation

The role of bile salts in liver regeneration

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