ABSTRACT
Objective To explore the role of Th17-and Treg-derived catecholamines during collagen-induced ar?thritis (CIA) progression. Methods Eighteen male DBA/1 mice were randomly divided into control group, CIA model groupⅠ(day 35) and CIA model groupⅡ(day 55). The CIA models were induced by typeⅡcollagen (CⅡ) injection from tails. mRNA expression of Th17 specific transcription factor include ROR-γt, cytokines, IL-17 IL-22, Treg specific transcription factor, Foxp3, cytokines, TGF-βand tyrosine hydroxylase (TH) in lymph nodes were examined by real-time PCR. Co-local?ization of ROR-γt or Foxp3, with TH, vesicular monoamine transporter-2 (VMAT-2) or monoamine oxidase (MAO) in lymph nodes were observed by immunofluorescence staining. Results In lymph nodes of mice in CIAⅠgroup and CIAⅡgroup, mRNA expression of ROR-γt, IL-17, TH and IL-22 were upregulated, while mRNA expression of Foxp3 and TGF-βex?pression was downregulated compared to those expression in control group. The upregulated expression of IL-17 was signifi?cantly reduced in CIAⅡgroup compared with that in CIAⅠgroup. In the lymph nodes of both intact and CIA mice, co-lo?calization of ROR-γt or Foxp3 with TH, VMAT-2 or MAO was seen in some cells. The numbers of cells that are double-pos?itive of ROR-γt/TH,ROR-γt/VMAT-2 and ROR-γt/MAO IL-17 were increased in CIA groups compared to those in con?trol group. And they are significantly reduced in CIAⅡgroup compared with those in CIAⅠgroup. Conclusion The abili?ty to synthesize catecholamines in Th17 cells was increased in lymph node in mice from CIA groups compared to that in con?trol group. The increased catecholamines production from Th17 cells in lymph nodes may be involved in the anti-inflammato?ry progression in CIA.
ABSTRACT
Objective To explore changes of expression of pro-and anti-inflammatory cytokines in the hippocam-pus of Aβ1-42-induced Alzheimer’s disease (AD) rat model. Methods Twenty-four SD rats were divided into control group, PBS group (PBS was injected into CA1 area of hippocampus) and AD model group (Aβ1-42 was injected into CA1 area of hip-pocampus). The escape latency was evaluated by Morris water maze in three groups. Nissl staining was used to detect the le-sions of hippocampal CA1 neurons. Levels of amyloid precursor protein (APP) and protein phosphatase 2A (PP2A) in hippo-campus were measured by Western blot analysis. Real-time PCR was employed to examine the expressions of pro-inflamma-tory cytokines, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ), and the mRNA expressions of anti-inflammatory cytokines, including IL-4, IL-10 and transforming growth factor-β(TGF-β). Re-sults Rats subjected to Aβ1-42 injection in bilateral hippocampus led to a ability reduction of learning and memory, a loss of neurons in hippocampus and an increase in the expression of APP, and a decrease in PP2A expression in the hippocampus. In AD hippocampus, The mRNA expressions of the pro-inflammatory mediator, IL-1β, TNF-αand IFN-γ, were significant-ly up-regulated, but the expressions of the anti-inflammatory cytokines, IL-4, IL-10 and TGF-β, were markedly down-reg-ulated in AD group compared with those of control and PBS groups. Conclusion The pro-inflammatory/anti-inflammatory imbalance induced neuro-inflammation in AD rats, which was involved in pathogenesis of AD.
ABSTRACT
Objective : To investigate the efficacy and safty of radiofrequency ablation for arrhythmia. Methods: The clinical data of 1 065 patients with arrhythmia by Radiofrequency ablation treatment were analyzed retrospectively, including 537 cases of atrioventricular nodal reentrant tachycardia, 386 cases of atrioventricular reentrant tachycardia, 59 cases of ventricular premature, 26 cases of ventricular tachycardia, 35 cases of atrial flutter, and 8 cases of paroxysmal atrial fibrillation. Results:The procedural succeed rate was 96. 80% , and complication was 1. 56%. Conclusion: Radiofrequency ablation was an safe and effective method in treating arrhythmia.