Dyslipidemia is commonly seen in human immunodeficiency virus (HIV) infected patients. Understanding the risk factors of abnormal lipid profiles is urgent for proposing targeted approaches to prevention. Our objective was to assess the incidence and associated factors of abnormal lipid profiles and atherogenic index of plasma (AIP) among antiretroviral therapy (ART) naïve men who have sex with men (MSM) acute HIV infection (AHI) and chronic HIV infection (CHI) patients in China.

Interleukin (IL)-27 is an IL-12 family cytokine and exerts a critical role in immune regulation in the context of infection, autoimmunity, and angiogenesis. In this study, we aimed to investigate the possible pathophysiological role of IL-27 and vascular endothelial growth factor (VEGF) in ankylosing spondylitis (AS). One hundred and forty AS patients and 90 healthy controls were included in the current study. The levels of IL-27 and VEGF in serum and synovial fluid (SF) samples were measured by enzyme-linked immunosorbent assay. Erythrocyte sedimentation rate, C-reactive protein, and human leukocyte antigen (HLA)-B27 were measured by standard laboratory techniques. Disease activity in AS was scored with Bath Ankylosing Spondylitis Disease Activity Index (BASDAI). Hip involvement, peripheral arthritis, and eye involvement were also recorded. The serum levels of IL-27 were remarkably higher in AS patients than healthy groups and significantly correlated with serum levels of VEGF. Furthermore, the serum levels of IL-27 were correlated with BASDAI independent of other markers of inflammation. Elevated serum levels of IL-27 and VEGF were detected in AS patients with peripheral arthritis and HLA-B27 positive. The SF levels of IL-27 and VEGF were significantly higher than serum levels in AS patients with peripheral arthritis. By contrast, levels of IL-27 and VEGF were not increased in AS patients with hip involvement and eye involvement. IL-27 may regulate the immunological or inflammatory process of AS.

目的 通过检测强直性脊柱炎(AS)患者血清中的白细胞介素27(IL-27)的水平,探讨其在AS发病的作用.方法 收集AS患者90例,采用双抗体夹心ELISA测定血清中的IL-27水平,并与30例健康对照者进行比较,同时测定红细胞沉降率(ESR)、C-反应蛋白(CRP)及Bath强直性脊柱炎疾病活动指数(BASDAI).结果 AS患者组血清IL-27水平为(603.4±76.2) pg/mL,明显高于健康对照组[(63.4±5.9) pg/mL,P＜ 0.001];且血清IL-27水平与ESR、CRP及BASDAI成正相关(r值分别为0.306、0.299、0.218,P分别为0.003、0.004、0.040).结论 IL-27可能参与了AS炎症与免疫反应.

Scutellarin inhibits hypoxia-induced and moderately high glucose-induced proliferation and vascular endothelial growth factor (VEGF) expression in human retinal endothelial cells (HRECs); thus, it could be a potential therapy for diabetic retinopathy. However, how scutellarin inhibits VEGF is unknown. In our study, HRECs were treated with high glucose and/or hypoxia-mimetic agent cobalt chloride to stimulate cell proliferation, migration, and angiogenesis, and the effects of scutellarin on these processes were analyzed through cell viability assay, Transwell migration assay and endothelial tube formation assay, respectively. The inhibition of angiogenic factor VEGF by scutellarin was confirmed by reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay. The mechanisms for VEGF inhibition were examined by luciferase reporter assay, Western blot, immunoprecipitation, and biochemical assays. We found that scutellarin not only concentration-dependently inhibited cell proliferation, migration, and tube formation in HRECs but also decreased their production of VEGF. The reduction of VEGF was due to increased ubiquitination and degradation of hypoxia-inducible factor (HIF)-1 alpha by scutellarin. Furthermore, scutellarin impaired the interaction of HIF-1 alpha with p300, which further decreased the transcriptional activity of HIF-1 alpha. As an inducer of HIF-1 alpha, oxidative stress was attenuated by scutellarin. Our data demonstrate that scutellarin exhibits an antiangiogenic effect via inhibition of oxidative stress, enhancement of HIF-1 alpha degradation, and reduction of VEGF secretion.

OBJECTIVE:Interleukin (IL)-33 is a cytokine belonging to the IL-1 family and was recently identified as a ligand for ST2, which belongs to the IL-1 receptor (IL-1R) family. In this study, we aimed to investigate the possible pathophysiological role of IL-33/sST2 in ankylosing spondylitis (AS).METHODS:The levels of IL-33/sST2 and vascular endothelial growth factor in serum samples of 140 patients with AS and 90 controls were measured by enzyme-linked immunosorbent assay. Erythrocyte sedimentation rate, C-reactive protein level, and human leukocyte antigen B27 were measured by standard laboratory techniques. Disease activity in AS was measured by the Bath Ankylosing Spondylitis Disease Activity Index. Hip involvement, peripheral arthritis, and eye involvement were also recorded.RESULTS:The serum levels of IL-33/sST2 were remarkably higher in the patients with AS than the healthy groups and significantly correlated with vascular endothelial growth factor and the Bath Ankylosing Spondylitis Disease Activity Index. The sST2 levels correlated with erythrocyte sedimentation rate, C-reactive protein, platelet, and human leukocyte antigen B27. Elevated levels of IL-33/sST2 were detected in the patients with peripheral arthritis, and sST2 were detected to be increased in the patients with hip involvement. By contrast, levels of IL-33 but not sST2 increased in the patients with eye involvement.CONCLUSION:IL-33/sST2 may regulate the immunological or inflammatory process of AS.