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This study was designed to explore the effect of apigenin (Api) on dendritic cell (DCs) maturation and function in murine spleen cells. The single spleen cell was isolated, and then cultured with lipopolysaccharide (LPS) in the present and absence of apigenin. After 24 h, the toxicity of Api and the T cell proliferation were determined by CCK8 kit. In addition, we collected the cell-free supernatants to measure cytokine production using ELISA, collected the cells to determine the DC maturation using flow cytometry. Finally, we purified Api and/or LPS-treated CD11c+ DCs which were pulsed with ovalbumin (OVA)323-339 and then were adoptive transferred into C57BL/6 mice to detect the OVA323-339-specific T cell proliferation and T helper (Th1) and Th2 cell secreting IFN-γ and IL-4 production, respectively. We found that Api did not affect splenocyte viability, but inhibited the production of pro-inflammatory cytokine IL-1β, IL-6 and TNF-α, not anti-inflammatory cytokine IL-10. In addition, Api inhibited the expression of co-stimulatory CD80, CD86 and MHCII of CD11c+ DCs. Finally, compared to LPS+OVA DCs group, DCs from Api and LPS co-treated splenocytes (Api+LPS+DCs) impaired OVA323-339-specific T cell proliferation and the production of IFN-γ and IL-4 in CD4+ T cells, which had the similar responses with OVA+DCs. These data suggest that Api exhibits anti-inflammatory properties via inhibiting DC activation and function, as a new immune-modulator, which may induce immune-tolerance with a benefit to those with chronic inflammation.
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<p><b>OBJECTIVE</b>To investigate the effect of transcriptional regulation of aberrant transcription factor AML1-ETO on p14.</p><p><b>METHODS</b>P14expression both in AML1-ETO-expressing cells or U937 nonexpressing cells and in leukemia cells of AML patients with or without t(8;21) was assessed by quantitative PCR. Methylation-specific polymerase chain reaction (MSP) was used to analyze the methylation status of p14promoter. The chromatin immunoprecipitation (ChIP)-based PCR was used to investigate the direct interaction between the AML1-ETO and p14promoter in AML1-ETO positive leukemia cell line. And the p14mRNA expression level was detected by qRT-PCR after treatment with 5-Aza.</p><p><b>RESULTS</b>AML1-ETO-expressing cell subclone displayed low level of p14mRNA in comparison with the non-transfected U937. In primary bone marrow cells of acute myeloid leukemia containing AML1-ETO, level of p14mRNA was markedly lower when compared with other acute myeloid leukemias lacking this translocation. P14gene promoter was non-methylated in control group and primary leukemia cells of AML patients without t(8;21) and was hyper-methylated in U937-A/E1-4 and primary leukemia cells of AML patients with t(8;21). The enriched regions in transfected cells were located within p14promoter. 5-Aza could increase the expression of p14.</p><p><b>CONCLUSION</b>P14is a possible target gene of AML1-ETO. The p14silencing induced by hyper-methlylation may be an important factor for occurrence and development of the Msubtype of acute myeloid leukemia.</p>
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AlM: To observe the effect of anterior chamber depth and angle change after pterygium excision.METHODS:Thirty cases (30 eyes) of primary pterygium were underwent pterygium excision. Central anterior chamber depth, four direction angle open distance ( AOD ) and open angle ( AA ) were measured preoperatively and postoperatively by ultrasound biomicroscopy ( UBM ) and the intraocular pressure was observed.RESULTS:Preoperative and Postoperative intraocular pressure were 15. 17±10. 6 and 16. 23±2. 61mmHg, and the central anterior chamber depth were 2. 28±0. 39 and 2. 33± 0. 24mm. The four directions of AOD and AA were no statistical difference.CONCLUSlON:The anterior chamber depth and the angle change is not obvious after pterygium excision.
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AIM:To evaluate the feasibility and significance of nasal endoscope combined with Neodymium-doped Yttrium Aluminium Garnet ( Nd:YAG ) laser in the treatment of recurrent dacryocystitis. METHODS: Forty-eight cases (48 eyes) with recurrent dacryocystitis were treated by nasal endoscope combined with Nd:YAG laser. The tubes were kept in place for 3-6mo after operation. The follow-up time was 3-18mo.RESULTS: Symptoms was completely resolved in 46 eyes and improved in 2 eyes, the cure rate was 100%. There were no other complications. CONCLUSION: Nasal endoscope combined with Nd:YAG laser provides an ideal therapeutic for recurrent dacryocystitis because of its many advantages such as a few complications, simple operation, no scars on face and so on and is fit for clinical application in primary hospitals.
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Objective To investigate the effect of all-trans retinoic acid(ATRA) on the expressions of Prohibitin1 (PHB1) and Prohi-bitin2 (PHB2) in hypoxic damage of renal tubular epithelial cells (RTEC).Methods Rat proximal tubular epithelial cell line NRK-52E culture was performed in the 37 ℃ 50 mL/L carbon dioxide incubator with mixture medium of fetal bovine serum and double-antibody(100 mL medium plus 5 mL fetal calf serum and 1 mL double-antibody).After 3 times cell propagation,the cells were divided into 3 groups:normal group,model group and ATRA intervention group.The normal group wasn't disposed,and the model group was put into vacuum tank filled with hypoxic gas(950 mL/L nitrogen and 50 mL/L carbon dioxide) to induce a hypoxic damage of RTEC.The ATRA intervention group was added 0.1 μmol/L ATRA and was treated with hypoxic gas as model group.After 24 h and 36 h,the mRNA expressions of PHB1,PHB2 and transforming growth factor-β1 (TGF-β1) were measured by using real-time PCR method,and the protein expressions of PHB1,PHB2 and TGF-β1 were detected by using Western blot method.Results 1.Compared with normal group,NRK-52E cells PHB1,PHB2 protein expressions and mRNA expressions at 2time points(24 h,36 h) were significantly decreased in model group and ATRA intervention group (all P ＜ 0.05),and the longer hypoxia time,the lower expression value.Compared with model group,NRK-52E cells PHB1 and PHB2 protein expressions and mRNA expressions in ATRA intervention group were increased significantly at 2 time points (all P ＜ O.05).2.Compared with normal group,NRK-52E cells TGF-β1 expressions and mRNA expressions at 2 time points(24 h,36 h) were significantly increased in model group and ATRA intervention group(all P ＜ 0.05),and the longer hypoxia time,the higher expression value;Compared with model group,NRK-52E cells TGF-β1 protein expressions and mRNA expressions in ATRA intervention group were decreased significantly at 2 time points(all P ＜ 0.05).Conclusions ATRA can significantly up-regulate the mRNA expressions and protein expressions of PHB1 and PHB2 in hypoxic damage of RTEC,and ATRA may have a protective effect against hypoxic damage.
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This study was aimed to investigate the effect of AML1-ETO fusion protein on the anti-apoptotic gene BCL-2 in leukemic cells and to explore its role in leukemogenesis. The apoptotic levels of U937-WT, U937-Mock and U937-A/E1-4 cells were examined by flow cytometry. And cleaved caspase-3 protein expression was detected by Western blot. BCL-2 gene expression both in AML1-ETO-expressing cells or U937 nonexpressing cells and in leukemia cells of AML patients with or without t(8;21) was assessed by quantitative PCR. The chromatin immunoprecipitation (ChIP)-based PCR was used to investigate the direct interaction between the AML1-ETO and BCL-2 promoter in AML1-ETO positive leukemia cell line. The results indicated that in U937-A/E cells but not in U937-WT or U937-Mock cells, apoptotic cells statistically significantly increased, and AML1-ETO expression also significantly enhanced activation of caspase-3. AML1-ETO-expressing cell subclones displayed significantly low levels of BCL-2 mRNA in comparison with the non-transfected U937. In primary bone marrow cells of acute myeloid leukemia containing AML1-ETO, levels of BCL-2 mRNA were markedly lower as compared with other acute myeloid leukemias lacking this translocation. The enriched regions in transfected cells were located within BCL-2 promoter. It is concluded that BCL-2 is the direct target gene of AML1-ETO. AML1-ETO can down-regulate the expression of BCL-2.