Changes of glycosaminoglycans in cerebrum, brainstem and cerebellum were measured in rats with hepatic encephalopathy induced by thioacetamide. It was foundthat the contents of glycosaminoglycans in brainstem and cerebrum were lowered markedlythan that of the normal control, but no significant difference of glycosaminoglycans werefound in cerebellum. The results suggested that the metabolism of glycosaminoglycans incerebrum and brainstem was disturbed when hepatic encephalopathy occured, and thatthe pathogenic mechanism of hepatic encephalopathy was related to the alterations of gly-cosaminoglycans in brain as a result of hepatic insufficiency.

Changes of pulmonary vascular permeability and blood gas were measuredin rats of experimental fulminant hepatic failure induced by thioacetamide. The resultsshowed that the pulmonary vascular permeability to Evans Blue in rats of fulminant he-patic failure with hepatic enphalopathy was markedly increased than that of normalcontrols (P

Objective To study the level and clinical significance of serum interleukin-18(IL-18)in patients with acute cerebral infarction.Methods The level of serum IL-18 in patient with acute cerebral infarction(n=90)and normal controls group(n=45)were detected by enzyme linked immunosorbent assay.Results The level of serum IL-18 in large,medium and small lesion group were(288.4±59.3);(237.5±58.0);(186.9±50.6)ng/L respeetlvely,which were significantly higher than those in normal control group.The level of serum IL-18 in control group was(147.2±42.8)ng/L(P＜0.05).large lesion group was significantly higher than that in medium and small lesion group(P＜0.05).medium lesion grouP was significantly higher than that in small lesion group(P＜0.05).The levd of serum IL-18 in heavy,medium and light group were(284.9±57.3);(233.4±55.9);(184.5±48.3)ng/L respectively,which were significantly higher than those in normal control group(P＜0.05);heavy group was slgnificantly higher than that in medium and light group(P＜0.05),medium group was significantly higher than that in light group(P＜0.05).Conclusion The level of serum IL-18 was related to the severity of cerebral infarction,IL-18 may be involved in the pathogenesis of the hypoxic ischemic brain injury.

AIM:To investigate the effects of antioxidant N-acetylcysteine(NAC)on the lipopolysaccharide(LPS)-induced MAPK phosphorylation in mouse liver.METHODS:54 male mice were divided into three groups:control(n=6),0.9% sodium chloride 0.2 mL ip;LPS group(n=24):LPS 5 mg ip;NAC+LPS group(n=24):NAC 150 mg?kg-1?d-1 ip,for 3 d;LPS 5 mg ip after 1 h of NAC administration at 3rd day.The liver was excised with carbrital anesthesia after LPS or 0.9 % sodium chloride injection at 0.5 h,1 h,2 h and 6 h for GSH and MDA assays.The protein extracted from liver was assayed for the phosphorylation of MEK1/2,ERK1/2,p38 MAPK by Western blotting.TNF-? in liver was assayed by radioimmunoassay.RESULTS:MDA in the liver was decreased remarkably and the GSH in the liver was increased significantly by NAC pretreatment.The phosphorylation of MEK1/2,ERK1/2 and p38 MAPK in liver were inhibited significantly by NAC pretreatment after LPS challenge.Meanwhile,TNF-? in liver was decreased markedly.CONCLUSION:Reactive oxygen species plays a critical role in MAPK signaling during the LPS induced acute liver injury.NAC partially inhibits LPS-induced MAPK signaling by antioxidant effect and decreases TNF-? production.

AIM:To investigate the effect of lipopolysaccharides(LPS)preconditioning on CCl4-induced liver injury and the change of LPS signal transduction.METHODS:The male Wistar rats were divided randomly into liver-injury group,which were injected with CCl4 5 mL/kg first,three days later were injected 0.3 mL 40% CCl4 and 60% olive oil. Animals in LPS preconditioning group were injected with LPS 0.5 mg/kg before the day CCl4 was given. Rats received high fat diet were as liver injury group,and normal control group received normal diet. The lymphocytes infiltrated in the liver tissue were counted. The endotoxin and ALT level in rat plasma,TNF-? content and expressions of TLR4,p38,p-p38,I??,NF-?? in the rat livers were also determined.RESULTS:The lymphocytes in liver slice and ALT level of the plasma in LPS preconditioning group were lower significantly than those in the liver injury group,and the expressions of TLR4,p-p38,NF-?? in the liver were the same. In contrast,the expression of I?? was higher.CONCLUSION:LPS preconditioning relieves obviously CCl4-induced chronic liver injury. The mechanism may be associated with change of signal transduction of LPS,which results in decrease of pre-inflammatory cytokines.

AIM: To investigate the effect of LPS on phagocytosis of Kupffer cells in vitro. METHODS: Isolated Kupffer cells were treated with LPS in vitro . The phagocytosis, microfilament, microtubules and apoptosis of Kupffer cells were determined by the beads phagocytosis test, fluorescence staining, fluorometry and flow cytometric analysis. RESULTS: LPS enhances the phagocytosis, actin content, microtubules fluorescence density of Kupffer cells in vitro , while at a large dose or for a long time, it lessened the phagocytosis increasing or phagocytosis, inhibites the microfilament and microtubules expression, and induced apoptosis. CONCLUSION: LPS enhances the phagocytosis of Kupffer cells in vitro , but in large amount, it inhibites the phagocytosis of Kupffer cells, which is probably related to LPS -induced microfilament, microtubules expression changes and apoptosis in Kupffer cells.

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.

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 role of methylated DNA mismatch repair gene MLH1 and MSH2 in the acquired multidrug-resistance of human small cell lung cancer cells H446.Methods The reverse transcription polymerase chain reaction(RT-PCR)and Western blot were applied to measure MLH1 and MSH2 mRNA and protein expressions of the multidrug-resistant cells H446/DDP and its parental cells H446.The promoter methylation status of the genes was assessed by methylation-specific PCR(MSP).Results The expressions of MLH1 and MSH2 significantly decreased both in mRNA level and protein level.Promoter methylation of MLH1 was observed in H446/DDP cells but not in H446 cells.Promoter semi-methylation of MSH2 in H446 cells was transformed to methylation in H446/DDP cells.Conclusion The downregulation of DNA mismatch repair gene MLH1 and MSH2 induced by its promoter methylation may play an important role in the acquired multidrug resistance of human small cell lung cancer.

OBJECTIVE:To study the chemical compositions of n-butabol extract from Solanum lyratum. METHODS:Glucan LH-20 column chromatography,silica gel column chromatography and TLC were adopted to separate and purity the chemical com-positions,physicochemical property and spectral evidence to identify their structures. RESULTS:Totally 10 chemical compositions were separated from n-butabol extract,namely apigenin-7-O-β-D-apiofuanosyl(1→2)-β-D-glucose (1),apigenin-7-O-β-D-glucose (2),adenosine(3),3-methoxy-4-hydroxy-5-[(8′S)-3′-methoxy-4′-hydroxyl-phenyl-alcohol]-E-cinnamic-phenylpropyl alcohol-4-O-β-D-glucoside (4),N-(4-amino-butyl)-3-(3-hydroxy-4-methoxy-phenyl)-E-acrylamide (5),N-(4-amino-butyl)-3-(3-hydroxy-4-me-thoxy-phenyl)-Z-acrylamide (6),resveratrol (7),naringenin (8),quercetin (9) and dioscin (10). CONCLUSIONS:Compound 1-8 are first separated from S. lyratum,the study can lay a foundation for quality evaluation of S. Lyratum.