Eph/ephrin signalling serves a bidirectional role in lipopolysaccharide­induced intestinal injury.

A growing body of evidence has demonstrated that Eph/ephrin signalling may serve a central role in intestinal diseases. However, whether erythropoietin­producing hepatocellular (Eph)/ephrin signalling is associated with the development of post­infectious irritable bowel syndrome (PI­IBS) is still unknown. In the present study, the role of Eph/Ephrin signalling in lipopolysaccharide (LPS)­induced intestinal injury was evaluated in vivo and in vitro. LPS treatment significantly increased the levels of proinflammatory mediators [monocyte chemoattractant protein­1, tumour necrosis factor α, interleukin (IL)­1ß, IL­6, intercellular adhesion molecule 1 and vascular cell adhesion molecule­1], activated the EphA2­Ephrin A1, protein kinase B (Akt)­nuclear factor (NF)­κB, Src­NF­κB and Wnt/ß­catenin signalling pathways, and inhibited EphB1­Ephrin B3 signalling in colon tissues, and primary cultured enteric neuronal and glial cells. Notably, EphA2 monoclonal antibody (mAb) treatment or Ephrin B3 overexpression could partially alleviate the LPS­induced upregulation of proinflammatory mediators, and Akt­NF­κB, Src­NF­κB and Wnt/ß­catenin signalling pathways. In addition, EphA2 mAb treatment could partially inhibit LPS­induced inactivation of EphB­Ephrin B3 signalling, while Ephrin B3 overexpression could abrogate LPS­induced activation of EphA2­Ephrin A1 signalling. EphB1/Ephrin B3 signalling may antagonise the EphA2/Ephrin A1­dependent pathway following LPS treatment. The results associated with the EphA2 signaling pathway, indicated that Eph/ephrin signalling may serve a bidirectional role in LPS­induced intestinal injury. Eph/ephrin signalling may be a novel therapeutic target for LPS­induced intestinal injury and potentially PI­IBS.

[Histopathological changes in rat transplanted hepatoma after lipiodol transarterial embolization].

OBJECTIVE: To study the histopathological effect of hepatic arterial infusion of lipiodol on transplanted hepatoma in rats. METHODS: Fourty-one rats bearing Walker-256 transplanted hepatoma were randomly divided into embolization group (n = 35, divided in 5 subgroups, with 7 rats in each) and control group (n = 6). Lipiodol (0.5 ml/kg)emulsified with 0.2 - 0.3 ml of 76% urografin (v:v = 1:1) was infused via gastroduodenal artery into hepatic artery in embolization group. Rats in the control group were given via the same route urografin only. Histopathological changes of the treated tumors were examined by light and transmission electron microscopy. RESULTS: In the control rats treated with urografin alone, the average tumor size increased 2.8 fold on day 3, while that in the lipiodol treated rats increased 1.7 fold (P < 0.01). Compared with the control group, on day 3, 5, 10 after embolization treatment, tumor necrosis was more extensive (P < 0.01). In one of the treated rats, the tumor was completely necrotic on day 10. Inflammatory reaction was marked in the early post-embolic period, but it was replaced by fibrous tissue encapsulation. From day 1 on, in 17 of the 18 treated rats, apoptotic cells, identified by typical morphology under light and electronic microscopes, were observed, mainly in the tumor periphery. CONCLUSION: In addition to cellular necrosis, apoptosis may be another important mechanism leading to cell death in hepatoma treated with transarterial embolization.

[Study on the pulmonary fibrogenetic effect induced by rush-mat dust in rats].

OBJECTIVE: To investigate the fibrogenetic effects induced by rush-mat dust in rats. METHODS: SD rats were treated with 50 mg of rush-mat dust per rat by intra-tracheal instillation, sacrificed 3, 6, and 12 months respectively after exposure. The lung tissue and lung lymph-node were taken out for pathological and electron microscopic examination. The content of collagen and ceruloplasmin (CP) in lung tissues were also determined. RESULTS: After treatment for 12 months, fresh wet lung weight in rush-mat dust group [(2.69 +/- 0.22) g] was higher than those in saline group [(1.87 +/- 0.25) g], TiO(2) group [(2.25 +/- 0.26) g], but lower than that in SiO(2) group [(11.41 +/- 1.63) g]; dry lung weight in rush-mat dust group [(0.47 +/- 0.03) g] was higher than those in saline group [(0.32 +/- 0.03) g], TiO(2) group [(0.41 +/- 0.08) g], but lower than that in SiO(2) group [(2.06 +/- 0.28) g]; lung collagen content in rush-mat dust group [(103.08 +/- 14.79) mg] was higher than those in saline group [(75.96 +/- 13.91) mg, TiO(2) group [(85.84 +/- 17.62) mg], but lower than that in SiO(2) group [(497.50 +/- 100.80) mg]; CP content in rush-mat dust group [(18.03 +/- 1.87) U/L] was higher than those in saline group [(15.05 +/- 2.24) U/L], TiO(2) group [(16.92 +/- 1.67) U/L], but lower than that in SiO(2) group [(25.37 +/- 3.58) U/L], P < 0.05 or P < 0.01. Pathological examination showed lung macrophage alveolitis, broadening of alveolar interval, one to two grade of silicotic nodes and increased amount of type II epithelial cell in alveolar as well as slight collagenous fibrosis in lung tissue of rush-mat dust group. Under electron microscope, primary and secondary lysosome and medullary sheath-like phagocytic residual body were found in lung tissue of rush-mat dust group, meanwhile the amount of type II alveolar epithelial cell and collagen fiber were slightly increased but these changes were less than those of quartz group. CONCLUSION: The rush-mat dusts have slight pulmonary fibrogenetic effect on rat.