AIM:To investigate LPS(lipopolysaccharide)stimulated cytokine secretion from normal rat kupffer cells in vitro. METHODS: Kupffer cells were isolated from wistar rats liver and cultured. Tumor necrosis factor - α (TNF- α) and endothelin- 1 (ET- 1 ) secreted by LPS stimulated kupffer cells were detected. RESULTS: LPS had an stimulative effect on kupffer cell activity. LPS in definite concentrations promoted kupffer cell secretion. CONCLUSION: LPS promotes kupffer cell secretion, which may be associated with liver injury induced by LPS.

AIM:To investigate LPS(lipopolysaccharide)stimulated cytokine secretion from normal rat kupffer cells in vitro. METHODS: Kupffer cells were isolated from wistar rats liver and cultured.Tumor necrosis factor -? (TNF-?) and endothelin-1(ET-1) secreted by LPS stimulated kupffer cells were detected. RESULTS: LPS had an stimulative effect on kupffer cell activity. LPS in definite concentrations promoted kupffer cell secretion.CONCLUSION: LPS promotes kupffer cell secretion, which may be associated with liver injury induced by LPS.

AIM:The objective of the study was to explore whether intestinal endotoxemia participate in the development of Alzheimer disease.METHODS:Adult Wistar rats were subjected to 90 days intraperitoneal injection with D-galactose and aluminum trichloride(AlCl3) to establish the model of Alzheimer disease.After the administration,the study and memory ability in the rats were observed by Morris water maze.The level of lipopolysaccharide(LPS) in the sera of Alzheimer disease's rats was determined by tachypleus amebocyte lysate method.The level of tumor necrosis factor-?(TNF-?) and interleukin-1(IL-1) in the sera were determined by radioimmunoassay.The expressions of amyloid ?-protein precursor(APP),presenilin 1(PS1) and ?-site APP-cleaving enzyme(BACE) in hippocampus were detected by RT-PCR.RESULTS:Compared with the normal control,the level of LPS in the sera and the expressions of APP,PSI,BACE mRNA in the hippocampus were markedly increased(P

AIM:To study the effect of intestinal endotoxemia(IETM) on hepatic energy metabolism in acute liver failure. METHODS:Intoxication by thioacetamide (TAA) was used to establish rat model of acute liver injury.Ketone body(acetoacetate and ?-hydroxybutyrate) in arterial blood and ATP content of hepatocellular mitochondria were determined by using enzymatic fluorimetric micromethod.Colectomy was adopted in observing the changes in plasma endotoxin content and serum alanine aminotransferase (ALT) activity. RESULTS:In the TAA group,plasma endotoxin content and serum ALT activity were all significantly higher than those in the control group(P

Objective To investigate the effect of hepatic microcirculatory disturbance induced by intestinal endotoxemia in liver injury. Methods The model of rats with intestinal endotoxemia induced by thioacetamide(TAA) was established. 25 Male Wistar rats were divided into 4 groups as normal control group (N), Heparin control group(H), TAA treated group(T), and TAA + heparin treated group(T +H). The changes of plasma biochemistry and hepatic histopathology were measured. Results The plasma endotoxin level, alanine transaminase (ALT) activity and malondialdehyde (MDA) content in TAA treated rats were markedly higher than that in the control ones (P < 0.05), while plasma endotoxin level was lower ( P > 0.05) and ALT as well as MDA were decreased significantly ( P < 0.05) in TAA + heparin group than in TAA group. Conclusion Intestinal endotoxemia could induce disturbance of hepatic microcirculation, which results in ischemia and hypoxia of liver cell. Heparin could not only correct disturbance of hepatic microcirculation induced by intestinal endotoxemia, but also reduce liver injury induced by ischemia and hypoxia.

0.05).Both HMGB1 mRNA expression and HMGB1 protein level were remarkably higher in LPS treatment group than that in control group(P0.05).CONCLUSION:RPM inhibits HMGB1 expression not only by directly suppressing STAT3 activation,but also by indirectly reducing TNF-? level.

AIM: To examine the effects of inhibition of Kupffer cell and splenectomy on intestinal endotoxemia and hepatic injury. METHODS: The hepatic injury model was established by treatment with thioacetamide (TAA). At the same time, inhibition of Kupffer cells by intravenous GdCl_3 and splenectomy were performed. Serum alanine aminotransferase (ALT), TNF-?, endotoxin content and phagocytic index were observed. RESULTS: In the TAA+GdCl_3 group, and TAA+splenectomy group, the endotoxin content was significently higher than that in normal and TAA group (P

Objectives To explore the relativity between Alzheimer ’ s disease ( AD)-like lesions and metabolic syndrome models induced by high-sugar high-fat diet in rats.Methods Forty-eight Sprague Dawley rats were randomly divided into 2 groups.The control group (fed with normal diet, 12 rats) and high sugar and high fat group (fed with high-sucrose and high-fat diet, 12 rats) continuously for 12 months.At the end of 6, 9 and 12 months of the experiment , we observed the animal body weight and visceral fat weight .The blood lipid levels , blood glucose and MS-related biochemical parameters were determined . The brain tissues were examined by histopathology . The characteristic AD molecules hippocampus Aβand Tau were detected using ELISA and Western blotting to confirm the presence of AD lesions in the brain.Results Compared with the normal control group , the body weight and visceral fat weight of the rats in the high-sugar high-fat groups were significantly increased; the levels of TG , FPG, LDL, HOMA-IR and hippocampus Aβ,phosphorylated Tau (p-Tau) were higher, but the level of HDL was decreased (P<0.05 for all).The histopathological examination revealed inflammatory cell infiltration in the brain tissues .Conclusions Characteristic AD-like lesions may occur and accompany the rat models of metabolic syndrome , induced by high-sugar high-fat diet, and provide a new idea for the construction of Alzheimer ’ s disease animal models .

Objective To investigate the effects of Shuangligan and Glycine on Thl/Th2 balancing on severe acute pancreatitis ( SAP) in rats. Methods Thirty-two Wistar rats weighing (260 ± 20) g were randomly divided into sham operation (SO) group, SAP group, SAP + Slg (with the treatment by Shuangligan) group and SAP + Gly (with the treatment by Glycine ) group. Each group included 8 rats, which accepted different treatment according to the experimental design. Changes of plasma level of endotoxin ( ET) and serum amylase (AMY) and the effects of Shuangligan and Glycine on Thl/Th2 ratio at the 24th hour after operation were observed respectively. Results The plasma endotoxin (ET) level ( (0. 67 ±0. 11) EU/ml),proinflammatory cytokine (INF-γ:(8.43 ± 0.86) ng/L, IL-12: (8.26 ± 1.97) ng/L) and Thl/Th2 ratio (0.36 ± 0.07) in SAP group were significantly higher than those in SO group( ET: (0. 44 ±0.07) EU/ml, INF-γ: (3. 80 ±0. 55) ng/L, IL-12: (3. 34 ± 1. 34)ng/L,Thl/Th2 ratio (0. 24 ±0. 05) ) (P <0. 05). Compared with SAP group, SAP + Slg and SAP + Gly group had remarkably decreased plasma ET level ( (0. 57 ± 0. 08,0. 52 ± 0. 04) EU/ml) (P < 0. 05) and the Thl/Th2 ratio reached equilibrium ( SAP + Slg group; (0. 29 ± 0. 04 ), SAP + Gly group: (0. 25 ± 0. 06 )) . Conclusions In the earlier stage of SAP, the rising plasma ET level may cause the overreaction of the cell mediated immune response, which leads to the aggravated damages in tissue cells. Our data indicates that Shuangligan and Glycine can restrain the formation of intestinal endotoxemia and alleviate or prevent the tissue injuries.

Objective To investigate the relationship between dendritic cell (DC)and intestinal endotoxemia in patients with chronic hepatitis B (CHB).Methods Peripheral blood were collected from CHB patients (n = 80)and healthy controls (n = 21 ).Plasma endotoxin (ET)levels,liver function (alanine transaminase,total bilirubin)were detected.According to plasma ET concentration,all CHB patients were divided into two groups:ET positive and ET negative.The peripheral blood mononuclear cells (PBMCs)were isolated and then cultured with recombinant human granulocyte-macrophage colony-stimulating factor ( rhGM-CSF),recombinant human interleukin-4 ( rhIL-4 ),FMS-related tyrosine kinase 3 ligand (Flt3L)and tumor necrosis factor-alpha (TNF-α)to derive DC.The phenotypic patterns were characterized by flow cytometry.The proliferation of T lymphocytes was evaluated with mixed leukocytes reaction (MLR)and the levels of IL-12 and interferon-γ (IFN-γ)produced by DC were analyzed with enzyme-linked immunosorbent assay (ELISA).Comparisons among the two groups and healthy control group were done by single factor analysis of variance.Results Compared to healthy controls,the expressions of CD83,CD80,CD86,human leucocyte antigen (HLA)-DR and the proliferation of allogeneic T lymphocytes by DC were all significantly reduced in CHB patient groups.The expressions of CD83,CD80,CD86,HLA-DR and the activation of proliferation in ET positive subjects were lower than those in ET negative subjects [CD83 (8.25±3.63)% vs(11.39±4.35)% ,CD80 (10.63±4.52)% vs (13.56±5.13)%,CD86 (36.61±16.16)% vs (45.90±15.35)%,HLA-DR (61.65±14.33)% vs (70.35±18.89)%,the activation of proliferation0.812±0.311 vs 1.153±0.324; F=5.123,4.213,3.714,3.323 and 3.125,respectively; all P＜0.05].After cultured for 9 days,the secretions of IL-12 and IFN-γ by DC were significantly lower in CHB patients than in healthy controls [IL-12 (16.99± 6.74)pg/mL vs (44.51±14.56)pg/mL,IFN-γ (10.52±4.19)pg/mL vs (17.94±5.86)pg/mL].The level of IL-12 in the ET positive group was significantly lower than that ET negative group [( 13.14 ±5.71)pg/mL vs (20.98 ± 9.03)pg/mL; F= 3.225,P = 0.016].The level of IFN-γ was not different between two groups [(9.46 ± 3.24)pg/mL vs (11.54 ± 5.20)pg/mL; F = 2.003,P =0.076].Conclusion The intestinal endotoxemia may play a role in DC dysfunction in CHB patients.