Anti-Hepatocyte Growth Factor polyclonal antibody

Periodontitis is a prevalent chronic inflammatory disease triggered by a synergistic and dysbiotic microbiota present in the oral biofilm. This in vitro study is aimed at evaluating the regulation of cyclooxygenase (COX)2 expression and production by the periodontopathogen Filifactor alocis in human gingival fibroblastic (HGF-1) and monocytic (THP-1) cells and also at investigating the underlying cellular pathway mechanisms. HGF-1 and THP-1 cells were exposed either to F. alocis or to the proinflammatory cytokine tumor necrosis factor alpha (TNF alpha) for 1 and 2 d to examine the COX2 expression by qPCR. COX2 protein levels were evaluated by ELISA in F. alocis-stimulated cells. Both types of cells were also stimulated with a blocking toll-like receptor (TLR)2 antibody or specific inhibitors against MAPKs. F. alocis significantly (p<0.05) increased COX2 at both transcriptional and protein levels in both HGF-1 and THP-1 cells. Moreover, the stimulatory effect of F. alocis on COX2 was more pronounced in HGF-1 cells in comparison to THP-1 cells. F. alocis upregulated the COX2 expression in a dose-dependent manner in both type cells at 1 d. TNF alpha also significantly (p<0.05) increased the COX2 expression in both cells. After preincubation of HGF-1 and THP-1 cells either with a neutralizing anti-TLR2 antibody or with specific MAPK inhibitors, the F. alocis-upregulated COX2 expression was significantly (p<0.05) suppressed at 1 d. Our in vitro study provides original evidence that F. alocis stimulates COX2 production in fibroblastic and monocytic cells through TLR2 and MAPK mechanisms, suggesting a role of this periodontopathogen in the etiopathogenesis of periodontitis.

We explored the feasibility of treating liver fibrosis with human Hepatocyte Growth Factor (HGF) carried by biotinylated ultrasound microbubbles plus biotinlated cationic nano-liposome composites (Bio-MB+Bio-CNLP) in bile duct-ligated (BDL) rats. In addition, we investigated the staging of hepatic fibrosis by using Perfusion-Weighted Imaging (PWI). We established a BDL rat model of hepatic fibrosis. HGF carrier was administered through tail-vein injections. The gene therapy efficacy was evaluated in vivo. Before and after treatment the rats were examined with MR-PWI. The perfusion parameters of PWl were compared with the fibrosis stage. The total fibrous tissue in the liver of rats treated with HGF was lower than that in control group. The time-signal intensity curve (TIC) peak of liver parenchyma of rats with hepatic fibrosis was characterized by a slow wash-in -out. A correlation was found between the perfusion parameters and the stage of fibrosis. As the stage of fibrosis increased, the wash-in and -out rates decreased progressively. The use of Bio-MB+Bio-CNLP is an effective and novel vector for gene delivery in vivo. Further, we confirm that HGF represents a valid liver anti-fibrotic molecule. PWI might be an effective method for quantifying the severity of liver fibrosis.