Clinicopathological significance of chemotactic factor IL-8, MCP-1 and MIP-1α expressions in gallbladder carcinoma

Objective：Gal bladder carcinoma was one of the malignant tumors in the digestive system, characterized by high recurrence and invasion. Recent research indicates that chemotactic factors such as IL-8, MCP-1 and MIP-1αhave played an important role in such aspects as formulation, growth, shifting of the tumor. The aim of this study was to investigate expressions of IL-8, MCP-1 and MIP-1αin gal bladder adenocarcinoma tissues. Methods：Gal bladder adenocarcinoma and noncancerous tissues were routinely formalin-fixed and paraf in-embedded, and in situ hybridization assay for IL-8, MCP-1 and MIP-1αmRNA. Results：（1） The positive rates or the scorings of IL-8, MCP-1 and MIP-1αmRNA were significantly higher in human gal bladder adenocarcinoma than those in human chronic cholecystitis （P〈0.01）. The positive rates or the scorings of three factors were lower in wel-dif erentiatiated gal bladder adenocarcinoma than in poorly-dif erenfiatted ones, whereas there was only one significant dif erence between MCP-1 mRNA （P〈0.05）. The closely positive correlation were found among IL-8, MCP-1 and MIP-1αmRNA. （2） Both the positive rates of IL-8 mRNA and MCP-1 mRNA as wel as their scorings were tightly related to their invasion of the common bile duct and the occurrence of lymph node transfer, moreover, the positive rates of MIP-1αmRNA and its scorings were tightly related to its invasion of liver. （3） Close positive correlation exists not only in IL-8 mRNA and MCP-1 mRNA （r=0.528）, but also in MIP-1αmRNA and IL-8 mRNA （r=0.422）, so does in MCP-1 mRNA and MIP-1αmRNA （r=0.638）. Conclusion：The positive rates or the scorings of IL-8, MCP-1 and MIP-1αmRNA are significantly higher in human gal bladder adenocarcinoma than those in human chronic cholecystitis, and the closely positive correlation are found among them, which suggests that IL-8, MCP-1 and MIP-1αregulate and influence the development and transformation of the gal bladder adencarcinoma together.

Identification of α7 nicotinic acetylcholine receptor on hippocampal astrocytes cultured in vitro and its role on inflammatory mediator secretion

The present study found expressions of a7 nicotinic acetylcholine receptor on hippocampal slices and hippocampal astrocytes using double immunofluorescence stainings. Expression of glial fibdllary acidic protein in the cultured hippocampal slices and hippocampal astrocytes significantly increased, and levels of macrophage inflammatory protein la, RANTES, interleukin-1β, intedeukin-6, and tumor necrosis factor-α increased in the supernatant of cultured astrocytes following exposure to 200 nM amyloid 13 protein 1-42. Preconditioning of 10 μM nicotine, a nicotinic acetylcholine receptor agonist, could attenuate the influence of amyloid β protein 1-42 in inflammatory mediator secretion of cultured astrocytes. Experimental findings indicated that α7 nicotinic acetylcholine receptor was expressed on the surface of hippocampal astrocytes, and activated a7 nicotinic acetylcholine receptor was shown to inhibit inflammation induced by amyloid β protein 1-42.

Tropism mechanism of stem cells targeting injured brain tissues by stromal cell-derived factor-1

Objective: To explore the role and function of stromal cell-derived factor- 1 (SDF- 1) in stem cells migrating into injured brain area.Methods: Rat-derived nerve stem cells (NSCs) were isolated and cultured routinely. Transwell system was used to observe the migration ability of NSCs into injured nerve cells. Immunocytochemistry was used to explore the expression of chemotactic factor receptor-4 (CXCR-4) in NSCs. In vivo, we applied immunofluorescence technique to observe the migration of NSCs into injured brain area. Immunofluorescence technique and Western blotting were used to test expression level of SDF- 1. After AMD3100 (a special chemical blocker) blocking CXCR-4, the migration ability of NSCs was tested in vivo and in vitro, respectively.Results: NSCs displayed specific tropism for injured nerve cells or traumatic brain area in vivo and in vitro. The expression level of SDF-1 in traumatic brain area increased remarkably and the expression level of CXCR-4 in the NSCs increased simultaneously. After AMD3100 blocking the expression of CXCR-4, the migration ability of NSCs decreased significantly both in vivo and in vitro.Conclusions: SDF-1 may play a key role in stem cells migrating into injured brain area through specially combining with CXCR-4.