ABSTRACT
Objective To investigate if the relative ratio between C1q and C3a, C5a had a relationship with the extent of coronary artery disease ( CAD) which had never been evaluated in humans.Methods Fifty-three patients scheduled for elective percutaneous coronary intervention ( PCI ) from February, 2016 to April, 2016 at Fuwai hospital were prospectively enrolled.According to the clinical and angiographic characters patients were divided into two groups:acute coronary syndrome ( ACS) group ( n=24), and control group (n=29, 19 patients with stable angina and 10 patients without CAD confirmed by angiography).In all individuals, fasting venous blood was collected by EDTA tubes after admission and strictly before PCI.The plasma level of C1q was measured by immune turbidimetric analysis, C3a and C5a were measured by ELISA tests.Differences between groups were assessed using t test, Mann-Whitney Utests, chi-squared test or Fisher exact test depending on the type of data respectively.Multivariate logistic regression analyses were conducted to evaluate the adjusted effect of C1q, C3a, C5a, C1q/C3a and C1q/C5a on ACS.Results Compared with control group, ACS group has an elevated circulation level of C3a (4 531.14 μg/L vs.4 179.95 μg/L, t=1.381,P=0.173) and C5a (6.44 μg/L vs.4.42 μg/L, t=0.133, P=0.108) but a decreased level of C1q (176.98 μg/ml vs.200.60 μg/ml, t=-2.022, P=0.048).The relative ratio of C1q/C3a was significantly decreased in ACS patients(4.05 ×10 -2 vs.4.97 × 10 -2 , t=-2.484, P=0.016).According to the multiple logistic regression analysis, lower relative ratio of C1q/C3a level proved to be independently associated with ACS ( OR=0.937, P=0.047, 95% CI:0.879-0.998).Conclusions The decreased relative ratio of C1q/C3a level proved to be independently associated with ACS.C1q/C3a ratio could be used as an important index reflecting the complement system homeostasis status which might have potential clinical value in evaluating the prognosis of patients with CAD.
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Objective:To detect the degree of oxidative stress in the process when Porphyromonas gin-givalis ( P. gingivalis) stimulates human vascular endothelium, And to investigate the effect of peroxi-some proliferator-activated receptor(PPAR)γ on oxidative stress during this process. Methods:Human vascular endothelial cells ( HVECs) line EA. hy926 ( American Type Culture Collection ,United States) was cultured in high glucose Dulbecco' s modified eagle medium ( DMEM) . Four groups were designed:control group, P. gingivalis infected group, PPARγactivated group and PPARγblocked group. In con-trol group HVECs were cultured with only DMEM. In P. gingivalis infected group, HVECs were time-dependently stimulated by P. gingivalis W83 from 0 to 12 h. In PPARγ activated group or PPARγblocked group, PPARγ was pre-activated or blocked by a representative PPARγ agonist(15d-PGJ2 10μmol/L) or antagonist ( GW966210μmol/L) 30 minutes before the cells were stimulated by P. gingiva-lis. At 0, 0. 5, 1, 1. 5, 2, 4, 8, and 12 h, the culture medium was collected individually and centri-fuged, and the supernatant was stored for assay. Glutathione peroxidase (GSH-PX) and malondialdehyde( MDA) were analysed by enzyme-linked immunosorbent assay. Cellular reactive oxygen species ( ROS) were detected through 2',7'-dichlorofluorescin diacetate (DCFA-DA) fluorescent probe at various time points of the different groups. Results:In P. gingivalis infected group, the levels of GSH-PX [(5. 56 ± 0. 97) μmol/L] and MDA [(0. 84 ± 0. 18) nmol/L] were significantly higher than those in control group [GSH-PX(4. 71 ± 0. 64) μmol/L, MDA (0. 59 ± 0. 18) nmol/L)]. The levels of GSH-PX and MDA in PPARγactivated group [GSH-PX (5. 38 ± 0. 84) μmol/L, MDA (0. 84 ± 0. 22) nmol/L] and in PPARγblocked group [GSH-PX (5. 37 ± 0. 76) μmol/L, MDA (0. 85 ± 0. 14) nmol/L] were signi-ficantly higher than those in control group (P <0. 05). In the PPARγ activated group, the levels of GSH-PX at 0 . 5 and 8 h were significantly higher than those from 1 . 5 h to 4 h ( P<0 . 05 ) , while no difference was observed on the MDA levels at different time points. There was no significant difference at various time points for the levels of GSH-PX and MDA in PPARγ blocked group. The level of cellular ROS detected by DCFH-DA in P. gingivalis infected group was significantly higher than that in control group (10 108. 65 ± 1 805. 18 vs. 6 049. 06 ± 1 199. 19,P<0. 05). No difference was observed be-tween PPARγ activated group (7 120. 94 ± 1 447. 30) or PPARγblocked group (6 727. 35 ± 1 483. 68) and control group. Conclusion:Oxidative stress happens when P. gingivalis stimulates human vascular endothelium. PPARγ may involve in modulating oxidative stress during this process.
ABSTRACT
Objective In order to study the effect of cold stress on the secretory function of rat ovary, the changes of hCG-induced progesterone and cAMP were observed and the livability of the oocytes was determined. Methods The rat luteal and granulose cells and the oocytes were cultured, progesterone and cAMP content was determined by radioimmunoassay kit (RIA kit) under 37 ℃, 0 ℃, -5 ℃, -10 ℃,-15 ℃, -20 ℃ and -25 ℃ respectively. The livability of the oocytes was determined by MTT assay. Results At -5 ℃ to -25 ℃, the content of progesterone in the luteal cells and granulose cells medium decreased compared with the control group. At 0 ℃～-25 ℃, the content of cAMP in the luteal cells and granulose cells medium was higher compared with the control. The livability of the oocytes was decreasing from -15 ℃. Conclusion Cold stress can inhibit hCG-induced progesterone secretion in the luteal and granulose cells of rats in the one hand, and can increase cAMP, decrease the livability of the oocytes in the other hand.