ABSTRACT
This study was aimed to observe the influence ofQing-Chang Hua-Shi Recipe (QHR) on IL-6trans-signaling in experimental colitis mice, in order to initially explore the possible mechanisms of QHR for ulcerative colitis (UC). TNBS/ethanol was used in the establishment of colitis mice model. After intervention of medication, ELISA was used in the detection of soluble Interleukin-6 receptor (sIL-6R). Real-time PCR was used to detect the mRNA expression level of IL-6 and glycoprotein 130 (gp130). Western blot was used in the observation of protein expression of IL-6 and gp130 in the colonic mucosa. The results showed that the level of sIL-6R, the mRNA and protein expression of IL-6 and gp130 in the model group were significantly higher than that in the control group. QHR was able to reduce the sIL-6R level (P < 0.01), decreased the mRNA and protein expression of IL-6 and gp130 (P < 0.01) in the colon tissues among experimental colitis mice. It was concluded that QHR had good anti-inflammatory effects on experimental colitis mice. It might be associated with influencing IL-6trans-signaling.
ABSTRACT
Objective To explore the mechanism of immunologic injury in patients with Tourette's syndrome(TS). Methods The serum level of anti-brain antibody ( ABAb) , antinuclear antibody ( ANAb) , soluble IL-6 receptor (sIL-6R) and soluble gpl30(sgp130) in patients with TS were analyzed by commercially available ELISA kits,and the titer of anti-streptolysin O ( ASO) in TS and in control was examined with latex enhanced immunoturbidimetry. Results The level of sIL-6R and sgpl30 was significantly elevated in TS compared with control group [(44. 1 ± 15.8)ng/mL vs (30. 3 ± 9. 0) ng/mL and (69. 0 ±24. 6)ng/mL vs (47. 3 ±14. l)ng/mL,P <0. 01 respectively]. ASO titer(250 U/mL) was found higher in TS than that in control(P <0. 01). The positive rates of anti-brain an-tibody and antinuclear antibody in TS were higher than that in control group (66% vs 4% and 53% vs 25% , P <0. 01 respectively). The level of ABAb negatively correlated with sgpl30 concentration( r = 0. 375, P <0. 05 ). Conclusion IL-6 signal transduction might be involved in Tourette's syndrome to lead the function enhancementand start cascade of feedback inhibition, because of elevated levels of slL-6R, sgp130, ANAb and ABAb in serum.Autoimmune-related injuries may potentially explain the pathogenesis of the disease.
ABSTRACT
BACKGROUND: Curcumin is a naturally occurring biologically active compound, and it has been shown to possess potent anti-inflammatory, anti-tumor and anti-oxidative properties. It is known for its anti-proliferative and proapoptotic effects in several cancer cells. Curcumin's effects on the mechanisms of cell survival and the expression of various cytokines were investigated in U266 cells and the in vivo effects of curcumin were examined using an animal model. METHODS: Cell proliferation assay and flow cytometry were used to examine cell proliferation, along with cell cycle analysis. The protein expressions were analyzed by Western blotting and the expressed levels of cytokines were analyzed by the ELISA method. RESULTS: Curcumin inhibited U266 cell growth in a dose-dependent and time-dependent manner. Cell cycle analysis showed an increased sub-G1 phase, a down regulated cyclinD1 expression and an induced p21 expression. Apoptosis induced a down regulated procaspase 3 expression and it induced cleaved PARP. Curcumin inhibited the IL (interleukin)-6 induced cell signal pathway via decreasing the STAT1 an 3, Erk cyclinD1 and c-myc expressions. Also, administration of 25mg/kg curcumin to a U266 animal model inhibited cancer cell engraftment in the bone marrow and it decreased the IL-6, sIL-6R and IL-8 expression levels. CONCLUSION: Curcumin induced cell cycle arrest and apoptosis and it inhibited the IL-6 mediated signal transduction pathways in U266 cells. Similar to the in vitro results, curcumin inhibited cancer cell proliferation and the expression of cytokine in vivo.
Subject(s)
Animals , Apoptosis , Blotting, Western , Bone Marrow , Caspase 3 , Cell Cycle , Cell Cycle Checkpoints , Cell Proliferation , Cell Survival , Curcumin , Cytokines , Enzyme-Linked Immunosorbent Assay , Flow Cytometry , Interleukin-6 , Interleukin-8 , Models, Animal , Multiple Myeloma , NF-kappa B , Peptides , Signal TransductionABSTRACT
BACKGROUND: The recognition of bronchial asthma as an inflammatory disease led to a search for soluble markers that would be useful in assessing airway inflammation. Interleukin-6 (IL-6) is a representative proinflammatory cytokine that has been shown to be connected with various inflammatory diseases. IL-6 acts via specific receptors that consist of the IL-6 binding glycoprotein gp80 and the signal transducer gp130. In the search for markers of airway inflammation, we investigated the role of soluble interleukin-6 receptor (sIL-6R) and IL-6 in acute asthma. METHODS: Serum levels of sIL-6R and IL-6 were measured in 78 acute asthmatics, in 15 patients with asymptomatic asthma and in 10 healthy control subjects by a specific ELISA using a murine antihuman IL-6R, IL-6 mAb (Quantikine sIL-6R, IL-6). RESULTS: Serum levels of IL-6 in acute asthmatics significantly exeeded those of control subjects. Those of sIL-6R in acute asthmatics were also significantly increased compared to those of control subjects. The serum concentration of IL-6 obtained in acute asthmatics was elevated as compared with the asymptomatic asthmatics. However, Association between eosinophilic count / IgE and IL-6 / sIL-6R in acute asthma could not found. CONCLUSION: Our results suggest that IL-6 may be involved in the pathogenesis of acute asthma and serum levels of IL-6 and sIL-6R may reflect the severity of airway inflammation.