Objective To investigate the role of glucocorticoid-induced tumor necrosis factor ligand (GITRL) in regulating the inflammatory reaction of kupffer cells.Methods The kupffer cells and T cells of mice were isolated and divided into 6 groups after being co-cultured:control group,kupffer cells and T cells were cultured in DMEM only; lipopolysaccharide (LPS) group,kupffer cells and T cells were cultured in media with LPS (1 mg/L) ; LPS + GITRL siRNA group,kupffer cells and T cells were cultured in media as the LPS group after transfected with GITRL siRNA ; LPS + control siRNA group,kupffer cells and T cells were cultured in media as the LPS group after transfected with control siRNA; LPS + pEGFP-N1 GITRL group,kupffer cells and T cells were cultured in media as the LPS group after transfected with pEGFP-N1 GITRL plasmid; LPS + pEGFP-N1 control group,kupffer cells and T cells were cultured in media as the LPS group after transfected with control plasmid.After 24 hours of treatment,the expressions of GITRL and PDL1 of kupffer cells were detected by immunofluorescence and western blot,respectively.The proliferation and apoptosis of T cells were measured by MTF assay and Annexin V/PI flow cytometry,respectively.The expression of tumor necrosis factor (TNF-α) in the supernatant fluid was measured by ELISA.All data were analyzed using the independent t test and one-way analysis of variance.Results The transfection efficiencies of GITRL siRNA and pEGFP-N1 GITRL were 90％ and 85％,respectively.Compared with normal kupffer cells,the protein expression of GITRL of kupffer cells transfected with GITRL siRNA was significantly decreased,while the protein expression of GITRL of kupffer cells transfected with pEGFP-N1 GITRL was significantly increased (t =41.72,13.10,P ＜ 0.05).There was no significant difference in the protein expressions of GITRL between normal kupffer cells and those in the control groups (F =2.27,P ＞ 0.05).The fluorescence intensity of GITRL in the LPS group was significantly higher than that in the control group (t =49.29,P ＜ 0.05).Compared with LPS group,the activation of GITRL expression by the LPS was significantly suppressed in the LPS + GITRL siRNA group (t =9.84,P ＜ 0.05),while the expression of GITRL in the LPS + pEGFP-N1 GITRL group was significantly increased (t =5.78,P ＜ 0.05).There was no significant difference in the GITRL expression among the LPS + control siRNA group,LPS + pEGFP-N1 control group and LPS group (F =0.86,P ＞ 0.05).The expression of PDL1 in the LPS group was significantly lower than that in the control group (t =18.83,P ＜0.05).Compared with LPS group,the expression of PDL1 in the LPS + pEGFP-N1 GITRL group was significantly suppressed (t =11.79,P ＜ 0.05),while the expression of PDL1 in the LPS + GITRL siRNA group was significantly stronger (t =19.08,P ＜ 0.05).There was no significantly difference in the expression of PDL1 in the LPS + control siRNA group,LPS + pEGFP-N1 control group and LPS group (F =2.22,P ＞ 0.05).The proliferation of T cells was increased and the number of apoptotic T cell was decreased in the LPS group when compared with control group (t =49.43,40.11,P ＜ 0.05).Compared with LPS group,the proliferation and apoptosis of T cells in the LPS + pEGFP-N1 GITRL group had the same trend (t =5.77,12.64,P ＜0.05); while the proliferation of T cells was decreased and the apoptosis of T cells was increased in the LPS + GITRL siRNA group (t =17.00,49.90,P ＜ 0.05).There was no significant difference in the proliferation and apoptosis of T cells among the LPS + control siRNA group,LPS + pEGFP-N1 control group and LPS group (F =1.87,1.35,P ＞ 0.05).The expression of TNF-α was significantly higher in the LPS group than that in the control group (t =125.68,P ＜ 0.05).Compared with the LPS group,the expression of TNF-α was significantly decreased in the LPS + GITRL siRNA group (t =119.65,P ＜ 0.05),while the expression of TNF-α in the LPS + pEGFP-N1 GITRL group was significantly increased (t =147.70,P ＜ 0.05).There was no significant difference in the TNF-α expression among the LPS + control siRNA group,LPS + pEGFP-N1 control group and LPS group (F =0.14,P ＞ 0.05).Conclusion Kupffer cells suppress the expression of PDL1 by upregulating GITRL,and thus activate the proliferation of T cells and promote the inflammatory reaction.The immunologic balance may be recovered after the interference of GITRL to restrain the inflammatory reaction.

Primary hepatic carcinoma is one of the common digestive tract tumors.Surgical operation in clinic is still the most effective way to treat it so far.The caudate lobe has often been considered the forbidden zone of hepatic operation in the past due to complicated anatomy.In resent years,with the deepening of knowledge of anatomy and advanced radiological technology,many new operative approachs and operation methods have been explored to improve the situation of caudate lobectomy which is already not rare in clinic now.This article summarized the anatomy of caudate lobe and reviewed the therapy progress of the hepatic carcinomas located caudate lobe.

Objective To study the protective mechanism of S-adenosylmethionine ( SAM) underlying liver injury induced by lipopolysaccharides ( LPS). Methods One hundred BABL/c mice were randomly divided into LPS group and SAM group. Mice in LPS group were intraperitoneally injected with 10 mg/kg LPS,and the mice in SAM group were injected with 100 mg/kg SAM 2 h before receiving the same dose of LPS. The survival rate of mice in 2 groups was recorded in 24,48,72 and 120 h after LPS injection. Histopathological changes in liver of mice were examined in 0,1,3,6,12 and 24 h after LPS injection. Tumor necrosis factor-? ( TNF-?) and interleukin-10 ( IL-10) levels in serum were measured by ELISA analysis at above time points. Expression of Toll-like receptor 4 ( TLR4) and liver X receptor ? ( LXR?) in hepatic tissues was detected by immunohistochemistry and Western blotting. Results SAM increased the survival rate of mice from 50. 0% ,40. 0% ,30. 0% ,and 30. 0% before LPS injection to 80. 0% ,70. 0% ,60. 0% ,and 50. 0% after its injection ( P

S-adenosylmethionine(SAM) is a physiologically active molecule in all the organizations and the human body fluids, and it is important to participate in a variety of biochemical reactions, the regulation of liver regeneration, liver cells differentiation and various sensitivity of the injury. The SAM affects the liver through a variety of ways. It is confirmed that the SAM and MTA can block the LPS-induced TNF-α of Kupffer cells to protect the liver. In a word, S-adenosylmethionine may be beneficial to LPS-induced liver in-jury in clinical treatment.

Primary gallbladder cancer is a relatively common biliarv malignant tumor but with a high mortality rate.Most patients with this disease reach an advanced stage when late onset symptoms occtur, and the prognosis tends to be poor even after radical operation.Searching for new diagnostic approaches of primary gallbladder, standardizing treatment strategy, conducting multieenter clinical trials of new drug, developing preventive measures according to different situations are significant methodls to improve the treatment effect prognosis.In this article, we reviewed the research progress of high risk factors, diagnostics, and treatment strategies of primary gallbladder cancer.

Objective To investigate the effect of gadolinium chloride (GdCl3) on the H22 experimental hepatocarcinogenesis in mice. Methods Totally 80 mice were inflicted to experimental hepatoma by implanting H22 cells to their liver lobes, and then equally and randomly divided into experimental hepatoma group (B) and GdCl3 pretreatment group (10 mg/kg, C). Another 40 mice served as normal control group (A). Ten mice from every group were killed respectively 7, 14, and 28 d after implantation. The left 10 mice were used for recording survival time and measuring the mass weight. Hepatic pathological histology was observed, and the expression of TNF-? was detected by ELISA and RT-PCR. Results ①Survival time was obviously higher in group B than in group C (P

In order to elucidate the mechanism of liver damage due to acute biliary sepsis,the changes of hepatocyte mitochondria were observed during biliary sepsis in the rat.The accompanied liver function changes were also studied.Mitochondrial calcium content,and lysosome fragility of the hepatocytes,lipid peroxide (LPO) level of liver tissue,ornithine carbamoytransferase (OCT),mitochondrial glulamicoxloacetic transaminase (m-GOT),and hepa-toplastin were determined.It was found that there were overloading of calcium in mitochondria,increase of lysosome fragility,and accumulation of LPO in the liver.These events would result in adverse effects on mitochondrial function.The activity of serum OCT and m-GOT was significantly increased,which suggests that mitochondria are seriously damaged since the 2 enzymes mainly come from hepatocyte mitochondria.And the liver reserving function declined progressively.Our study indicates that mitochondrial damage does exist during acute biliary sepsis,which might play an important role in liver damage.

The phagocytic function of Kupffer cells (KC) during acute obstructive cholangitis was observed in 244 Wistar rats.The rats were killed in the 6th,12th,24th,and 48th hour after operation,and the uptake of colloidal carbon by KC,plasma endotoxin and fibronectin(Fn)were determined and the morphology of KC was observed.It was found that in the rats with acute obstructive cholangitis,the phagocytic function of KC and plasma Fn significantly elevated in the 6th hour and markedly reduced in the 48th hour after operation as compared with those of the control (P

The pathological changes of the damages on many vital organs during acute obstructive cholangitis were observed in 45 rats under optical and electron microscopy.The morphological changes of the vital organs were characterized by disturbance of blood circulation,degeneration and/or necrosis of the tissues and cells,and inflammatory reactions.The hepatic damage appeared earlier and more severe thna the other organs during acute obstructive cholangitis.

Objective To investigate the mechanism of gadolinium chloride (GdCl3) inhibiting Kupffer cells (KCs) to suppress acute rejection following liver allograft transplantation in the rats. Methods The rats were randomly divided into control group (A), liver transplantation with GdCl3 pretreatment group (B), and liver transplantation with normal saline pretreatment group (C). The survival rate, liver function, hepatic pathological histology, cytokine level in liver and bile, activity of NF-?B in KCs, and membraneous molecules on the KCs were observed. Results (1) The one-month survival rate in group B was significantly higher than that in group C (P