ABSTRACT
BACKGROUND:We tried to combine 8-bromo-7-methoxychrysin and sorafenib in order to offset the tolerance of hepatocelular cancer stem cels to sorafenib, thereby comprehensively improving the therapeutic efficacy on hepatocelular carcinoma. OBJECTIVE:To observe the effects of 8-bromo-7-methoxychrysin, sorafenib and their combination on apoptosis of liver cancer stem-like cels SMMC-7721, and to analyze their mechanisms. METHODS:SMMC-7721 cels were treated with 8-bromo-7-methoxychrysin, sorafenib alone and their combination for 24 hours. Then, flow cytometry was used to detect cel apoptosis and western blot assay was used to determine nuclear factor-κB protein expression. RESULTS AND CONCLUSION:Compared with 8-bromo-7-methoxychrysin group and sorafenib group, the apoptotic rates of SMMC-7721 cels were significantly enhanced after treatment with the combination of 8-bromo-7-methoxychrysin group and sorafenib (2.5, 5, 10, 50 μmol/L), and meanwhile, the protein expression of nuclear factor-κB was down-regulated significantly. These findings indicate that the combined therapy of 8-bromo-7-methoxychrysin group and sorafenib can enhance the apoptosis of SMMC-7721 cels, which may be associated with down-regulation of nuclear factor-κB protein.
ABSTRACT
Auxotrophic strains of N1-37 (Phe-) and N2-27 (His-), screened from mutations of Paenibacillus polymyxa JSa-9 previously, were used as the parent strains to screen high-producing LI-F antibacterial lipopeptide fusion strain through protoplast fusion with polyethylene glycol as a promote agent. Fusion strain F5-15 was obtained. Then the product of LI-F antibacterial lipopeptide was quantified by HPLC, and the difference of expression of the key genes of lipopeptide synthase between wild strain JSa-9 and the fusion strain was analyzed by real-time PCR. LI-F antibacterial lipopeptide yield of the fusion strain F5-15 was 3.1-fold of the original strain JSa9's, and the expression levels of the target genes were 10.48, 2.48, 2.1 and 11.8 fold of the initial strain JSa-9, respectively.
Subject(s)
Anti-Bacterial Agents , Chromatography, High Pressure Liquid , Lipopeptides , Paenibacillus , Metabolism , Protoplasts , Metabolism , Real-Time Polymerase Chain ReactionABSTRACT
To explore the roles of tumor necrosis factor-alpha (TNF-alpha) and heat shock protein 60 (HSP-60) in women with tubal factor infertility (TFI) associated with Chlamydia trachomatis, and to determine the mechanisms of fallopian adhesions in Chlamydia trachomatis (CT) infections, the expressions of TNF-alpha and HSP-60 were quantitatively determined in 60 cases of TFI and 30 controls by immunohistochemical technique. The patients with TFI were further divided into group A and group B according to the CT-DNA of cervical specimens of PCR. The quantitative analysis was conducted by employing computerized image analysis system. It is found that the expressions of TNF-alpha and HSP-60 were much higher in TFI patients than those of controls. Among CT-HSP responders, a stronger expression was correlated with more severe salpingeal pathology. It is concluded that TNF-alpha and HSP-60 play very important roles in fallopian tube adhesion and occlusion in TFI due to CT infection.
Subject(s)
Adult , Female , Humans , Chaperonin 60 , Blood , Chlamydia Infections , Blood , Chlamydia trachomatis , Fallopian Tube Diseases , Virology , Infertility, Female , Metabolism , Tumor Necrosis Factor-alpha , MetabolismABSTRACT
AIM: The goal of the present study was to evaluate the possibility about enterogenous endotoxemia in pathogenesis of hepatopulmonary syndrome. METHODS: The rat model of cirrhosis was prepared with compound factors. A small dose of lipopolysaccharide (LPS) was administered intraperitoneally once to aggravate endotoxemia of animal with cirrhosis. The normal rats injected with LPS or injected with LPS combined with glycine (LPS antagonist) were designed as controls. RESULTS: Hepatopulmonary syndrome of rats with cirrhosis had occurred in the end of eighth weeks. Pulmonary pathological changes of cirrhosis rats were exacerbated after administration of a given dose of LPS. Glycine sharply antagonized the biological effect of LPS in vivo and in vitro, inhibited the production of TNF-? by LPS and alleviated various pathological changes of hepatopulmonary syndrome. CONCLUSIONS: Enterogenous endotoxemia in cirrhosis rats might be an important mechanism in the development of hepatopulmonary syndrome. Endotoxin and its mediating effect by way of cytokines (TNF-?) may play a role in the pathogenesis of hepatopulmonary syndrome.