LncRNA Snhg1 Plays an Important Role Sequestering rno-miR-139-5p to Function as a ceRNA in Acute Rejection After Rat Liver Transplantation Based on the Bioinformatics Analysis.

In order to explore the molecular mechanism of acute rejection after liver transplantation (ARLT) in rats, we employed the GSE36798 data set in the Gene Expression Omnibust (GEO) database to construct a related ceRNA network. This dataset contained a total of 16 samples (8 graft samples and 8 plasma samples). Each kind of sample was divided into acute rejection (AR) groups and non-acute rejection (NR) groups, and each group had 4 replicates.

Macrophage Membrane-Coated Nanoparticles Alleviate Hepatic Ischemia-Reperfusion Injury Caused by Orthotopic Liver Transplantation by Neutralizing Endotoxin.

Purpose: To investigate the effect and mechanism of macrophage membrane-coated nanoparticles (M-NPs) on hepatic ischemia-reperfusion injury (I/RI) caused by orthotopic liver transplantation. In addition, the advantages of TLR4/M-NPs compared to M-NPs are discussed.

Materials And Methods: We prepared biomimetic M-NPs and identified their characteristics.

Tauroursodeoxycholic acid alleviates hepatic ischemia reperfusion injury by suppressing the function of Kupffer cells in mice.

The aim of this study is to investigate the protective effect and the mechanism of tauroursodeoxycholic acid (TUDCA) against hepatic ischemia reperfusion (IR) injury. Male Balb/c mice were intraperitoneally injected with tauroursodeoxycholic acid (400 mg/kg) or saline solution, once per day for 3 days before surgery, and then the model of hepatic I/R injury was established. Blood and liver samples were collected from each group at 3, 6, and 24 h after surgery.

Fatty acid activates NLRP3 inflammasomes in mouse Kupffer cells through mitochondrial DNA release.

Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease in many developed and developing countries worldwide. It has been well established that the chronic sterile inflammation caused by the NLRP3 inflammasome is closely related to NAFLD development. Kupffer cells (KCs) are involved in the pathogenesis of various liver diseases.

Cathepsin B regulates non-canonical NLRP3 inflammasome pathway by modulating activation of caspase-11 in Kupffer cells.

Objectives: The non-canonical inflammasome pathway was described which engages caspase-11 to mediate pyroptosis and the subsequent release of IL-1α, IL-1β and IL-18 in TLR4-independent way. Cathepsin B is capable of activating caspase-11 under cell-free conditions which may regulate non-canonical NLRP3 inflammasome pathway. In this study, we aimed to further investigate cathepsin B as potential activators of proinflammatory caspases which may be released upon proinflammatory stimuli and regulate non-canonical NLRP3 inflammasome pathway by modulating the activity of caspase-11.

SIRT1 upregulation protects against liver injury induced by a HFD through inhibiting CD36 and the NF‑κB pathway in mouse kupffer cells.

Sirtuin 1 (SIRT1) is an NAD(+)‑dependent deacetylase, and a critical regulator in various metabolic processes, such as non‑alcoholic fatty liver disease (NAFLD). The present study aimed to investigate whether activating SIRT1 could modulate the CD36 and nuclear factor (NF)‑κB pathways to protect against liver injury induced by a high‑fat diet (HFD) in mice. A mouse NAFLD model was established by administration of a HFD for 8 weeks.

Investigation for role of tissue factor and blood coagulation system in severe acute pancreatitis and associated liver injury.

This study aims to investigate the molecular mechanisms underlying the pathogenesis of severe acute pancreatitis (SAP) and SAP-associated liver injury, we performed an association analysis of the functions of tissue factor (TF) and blood coagulation system in both SAP patients and mouse SAP model. Our results showed that serum TF and tissue factor-microparticle (TF-MP) levels were highly up-regulated in both SAP patients and SAP mouse model, which was accompanied by the dysfunction of blood coagulation system. Besides, TF expression was also highly up-regulated in the Kupffer cells (KCs) of SAP mouse model.

Bone marrow stromal cells attenuate LPS-induced mouse acute liver injury via the prostaglandin E 2-dependent repression of the NLRP3 inflammasome in Kupffer cells.

The nucleotide-binding and oligomerization domain-like receptor 3 (NLRP3) inflammasome participates in the pathogenesis of acute liver injury during sepsis. Bone marrow mesenchymal stem cells (BMSCs) attenuate sepsis through prostaglandin E 2 (PGE2) by increasing the interleukin-10 (IL-10) production of macrophages; moreover, NLRP3 inflammasome assembly is effectively regulated by IL-10 during infection. Whether BMSCs have an effect on the activation of the NLRP3 inflammasome and its underlying mechanism is unclear.

LXRα represses LPS-induced inflammatory responses by competing with IRF3 for GRIP1 in Kupffer cells.

Liver X receptors (LXRs) in the nucleus play important roles in lipid metabolism and inflammation. The mechanism of LXR regulation of the LPS-induced Toll-like receptor 4 (TLR4) inflammatory signaling pathway remains to be elucidated. C57/BL6 mice were randomly divided into four groups: control, T0901317 (a LXRs agonist), LPS and T0901317+LPS.

Effect of taurine on IRAK4 and NF-kappa B in Kupffer cells from rat liver grafts after ischemia-reperfusion injury.

Background: The aim of this study was to explore the protective mechanisms of taurine pretreatment against hepatic ischemia/reperfusion injury after liver transplantation.

Methods: A Sprague-Dawley-to-Sprague-Dawley rat liver transplantation model was used in this study. At 0, 60, and 180 minutes after reperfusion, expression of interleukin-1 receptor-associated kinase-4 (IRAK-4) messenger ribonucleic acid and protein in Kupffer cells was determined by real-time polymerase chain reaction and Western blotting.

Role of liver X receptors in cholesterol efflux and inflammatory signaling (review).

Liver X receptors (LXRs) are nuclear receptors that play a central role in cholesterol metabolism. When activated, LXRs induce a series of genes that are involved in cholesterol efflux, absorption, transport and excretion. In recent studies, LXRs have also been shown to play an important role in inflammatory signaling.

Prevention of common bile duct injury during laparoscopic cholecystectomy.

Background: Since the widespread adoption of laparoscopic cholecystectomy (LC) in the late 1980s, a rise in common bile duct (CBD) injury has been reported. We analyzed the factors contributing to a record of zero CBD injuries in 10 000 consecutive LCs.

Methods: The retrospective investigation included 10 000 patients who underwent LC from July 1992 to June 2007.

[Liver X receptor alpha inhibits LPS-induced inflammation by down-regulating IFR3 and GRIP1 in mouse Kupffer cells].

Objective: To explore the possible mechanism of the inhibitory effect of liver X receptor alpha (LXRalpha) on lipopolysaccharide (LPS)-induced inflammation in mouse Kupffer cells (KCs).

Methods: The KCs isolated from the liver of male KM mice and cultured in RPMI 1640 containing 20% FBS for 24 h were divided into control, LPS, T0901317, and LPS+T0901317 groups with corresponding treatments. The expressions of LXRalpha, interferon regulatory factor 3 (IRF3) and glucocorticoid receptor interacting protein 1 (GRIP1) in the KCs were detected by Western blotting.