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41.
42.
目的:观察IL-17、IL-22等细胞因子在PIA大鼠模型中的表达。方法:构建不同时间点的PIA模型,分别在D6、D12、D26和D70收集脾脏、滑膜及踝关节,用实时定量PCR的方法检测IL-17、IFN-γ、IL-22等细胞因子及细胞因子相关受体和转录因子在脾脏和滑膜中mRNA的表达水平。结果:在脾脏中,IL-17在D6和D26均有增高的趋势,但无统计学差异;IFN-1在D6和D26有增高的趋势,在D70表达显著升高;IL-22在D6、D12以及D70均较对照组显著升高。在滑膜中,IL-17、IL-17F以及IFN-γ的mRNA在D26组显著升高,而IL-22的表达在D70组显著上调。免疫组织化学方法检测IL-17、IL-21、IL-22以及IL-22R1在PIA模型中的表达部位。结果提示,在PIA踝关节中,IL-17主表达于浸润的炎性细胞上;IL-21和IL-22类似,不仅表达于浸润的炎性细胞中,在增殖层关节软骨或者修复过程中的新生软骨上也有表达;IL-22R1在PIA大鼠增生的滑膜的A型细胞和B型细胞中均有表达。结论:在PIA大鼠模型的脾脏及关节滑膜中,IL-22均主在疾病的慢性期升高更明显。 相似文献
43.
目的:研究 HGF 对人舌鳞癌 Tca8113细胞中 VEGF-C 表达的影响并探讨其作用机制。方法:体外培养 Tca8113细胞,应用 ELISA 方法测定不同浓度 HGF 作用下以及分别用 LY294002、U0126、SP600125、SB203580信号通路抑制剂阻断PI3K/Akt、P44/P22MAPK、JNK、P38MAPK 信号通路后 VEGF-C 的表达水平。结果:随着培养液中 HGF 浓度的增加,Tca8113细胞中 VEGF-C 的表达水平出现先增高后降低的趋势,当 HGF 浓度为40 ng/ml 时,VEGF-C 表达水平最高。PI3K/Akt 信号通路抑制剂(LY294002)和 P42/44MAPK 信号通路抑制剂(U0126)显著抑制了 HGF 刺激下 Tca8113的 VEGF-C 蛋白的表达(P <0.01);而 JNK 信号通路抑制剂(SP600125)和 P38MAPK 信号通路抑制剂(SB203580)对 HGF 刺激下 Tca8113的 VEGF-C 蛋白的表达影响甚微(P >0.05)。结论:在人舌鳞癌 Tca8113细胞中,随着 HGF 浓度的增加,VEGF-C 的表达先增高后降低。PI3K/Akt 和 P44/P22MAPK 信号通路在口腔鳞状细胞癌淋巴转移中可能发挥作用。 相似文献
44.
Hazel Turnbull D.J.H. Trafford H.L.J. Makin 《Clinica chimica acta; international journal of clinical chemistry》1982,120(1):65-76
A simple one step high-performance liquid Chromatographie (HPLC) procedure for the analysis of plasma concentrations of 25-hydroxyvitamin D3 (25-OHD3) and 25-hydroxyvitamin D2 (25-OHD2) is described. Plasma (2–4 ml) was extracted with methyl cyanide which was passed through a Sep-Pak C18 cartridge, washed with methanol: water (70:30, v/v) and the 25-OHD fraction eluted with methyl cyanide. After isomerisation to their isotachysterol derivatives, the secosteroids were estimated using a straight-phase HPLC system, monitoring the eluent at 301 nm. Radioactive 25-OHD3, added to plasma at the start of the procedure, was used to correct for losses. Recovery of added 25-OHD3 was quantitative and values obtained using this method were similar to those obtained on the same plasma samples using a mass fragmentographic technique. Normal ranges were similar to those described by other workers and within- (5.8% for 25-OHD3) and between- (8.0% for 25-OHD3) batch reproducibilities were satisfactory. 相似文献
45.
目的 探讨小檗碱对于Erastin诱导小鼠海马神经元HT22细胞的铁死亡的保护作用及其可能机制。方法 以HT22小鼠海马神经元细胞为研究对象,分为对照组、Erastin模型组、Erastin+30 μmol/L BBR组、Erastin+60 μmol/L BBR组。采用CCK-8法、特异性 Fe2+ 荧光探针、荧光染料(DAPI)检测和荧光探针(H2DCFH-DA)检测各实验组细胞的增殖情况、活性铁水平、细胞凋亡和活性氧(ROS)变化。 RT-qPCR和Western blot分别检测各实验组细胞的Nrf2、HO-1、GPX4 mRNA和蛋白表达情况。以60 μmol BBR的最适浓度来进一步探究其作用机制,分为对照组、Erastin模型组、Erastin+60 μmol/L BBR组、Erastin+60 μmol/LBBR+2 μmol Nrf2抑制剂 ML385组。通过使用荧光探针和Western blot检测Nrf2抑制剂(ML385)作用后的活性铁的水平、活性氧含量以及Nrf2、HO-1、GPX4蛋白的表达来验证小檗碱调节的Nrf2-HO-1/GPX4通路对Erastin处理的HT22细胞的保护作用。结果 0.5 μmol/L Erastin作用于HT22细胞8 h,细胞存活率与对照组相比显著被抑制(P<0.05);同时细胞凋亡、ROS以及活性铁含量增加(P<0.05)。与Erastin组比较,Erastin+30 μmol/L BBR组和Erastin+60 μmol/L BBR组的细胞存活率明显升高(P<0.05),同时显著降低细胞凋亡、ROS以及活性铁含量(P<0.05)。小檗碱增加 HT22细胞中Nrf2、HO-1、GPX4基因及蛋白的 表达量(P<0.05)。加入Nrf2抑制剂ML385后,Nrf2-HO-1/GPX4通路被抑制,并且ROS以及活性铁含量升高(P<0.05)。结论 Erastin诱导HT22细胞发生铁死亡,小檗碱抑制Erastin诱导的铁死亡,可能机制是激活了Nrf2-HO-1/GPX4通路。 相似文献
46.
47.
48.
H. Sasajima S. Miyagi Y. Kakizaki T. Kamei M. Unno S. Satomi M. Goto 《Transplantation proceedings》2018,50(9):2815-2820
Background
Liver transplantation from donors after cardiac death (DCD) might increase the pool of available organs. Recently, some investigators reported the potential use of mesenchymal stem cells (MSCs) to improve the outcome of liver transplantation from DCD. The aim of this study was to evaluate the cytoprotective effects and safety of MSC transplantation on liver grafts from DCD.Methods
Rats were divided into 4 groups (n = 5) as follows: 1. the heart-beating group, in which liver grafts were retrieved from heart-beating donors; 2. the DCD group, in which liver grafts were retrieved from DCD that had experienced apnea-induced agonal conditions; 3. the MSC-1 group, and 4. the MSC-2 group, in which liver grafts were retrieved as with the DCD group, but were infused MSCs (2.0 × 105 or 1.0 × 106, respectively). The retrieved livers were perfused with oxygenated Krebs-Henseleit bicarbonate buffer (37°C) through the portal vein for 2 hours after 6 hours of cold preservation. Perfusate, bile, and liver tissues were then investigated.Results
Bile production in the MSC-2 group was significantly improved compared with that in the DCD group. Based on histologic findings, narrowing of the sinusoidal space in the both MSC groups was improved compared with that in the DCD group.Conclusions
MSCs could protect the function of liver grafts from warm ischemia-reperfusion injury and improve the viability of DCD liver grafts. In addition, we found that the infusion of 1.0 × 106 MSCs does not obstruct the hepatic sinusoids of grafts from DCD. 相似文献49.
E. Karakulska-Prystupiuk J. Drozd-Sokołowska A. Waszczuk-Gajda A. Stefaniak J. Dwilewicz-Trojaczek A. Kulikowska E. Chmarzyńska-Mróz G. Basak M. Paluszewska P. Boguradzki W. Jędrzejczak 《Transplantation proceedings》2018,50(7):2212-2217
Background
Relapse is the leading cause of treatment failure for myeloid malignancies treated with allogeneic hematopoietic stem cell transplantation. Treatment options are very limited and use of azacitidine is one of the available options.Methods
This was a retrospective, single-institution study. Of 28 evaluated patients, 18 were males, and the median age was 60 years (range, 15–78). There were 15 patients with acute myeloid leukemia, 8 with myelodysplastic syndrome, 4 with chronic myelomonocytic leukemia, and 1 with primary myelofibrosis. Ten patients received azacitidine for overt relapse, 14 received it as a preemptive therapy, and 4 others received it as maintenance treatment after allo-hematopoietic cell transplant (HSCT). Eleven patients received a donor lymphocyte infusion (DLI).Results
The patients received median 5 (1–9) cycles of azacitidine in preemptive and maintenance therapy and median 2.5 (1–9) cycles in patients with relapse. Thirty-nine percent of patients received DLIs. Median overall survival was 6.1 months (95% CI, 0.7–13) for relapse therapy vs 21.2 months (95% CI, 8.4-inf) for preemptive therapy. Among patients treated for relapse, 30% achieved temporary disease control and underwent the second allo-HSCT. A complete, cytogenetic remission was achieved in 50% of patients and stable minimal residual disease in 14% of patients in a group with preemptive therapy. Toxicity was considerable; neutropenia (71%), anemia (14%), thrombocytopenia (36%), and serious infections (36%) were observed in the preemptive setting.Conclusions
These data support the notion that azacitidine is best used as a preemptive therapy against relapse for patients after allo-HSCT performed for myeloid malignancy. Applying azacitidine as therapy for ongoing relapse after allo-HSCT may lead to stable disease and allow for better performance of the second allo-HSCT. 相似文献50.
A. Pacek Ł. Czyżewski M. Saran J. Wyzgał Ł. Szarpak 《Transplantation proceedings》2018,50(6):1824-1828