Effect of PR-957 on the formation of A1 reactive astrocytes / 中国当代儿科杂志

OBJECTIVE@#To study the effect of PR-957 on the formation of A1 reactive astrocytes.@*METHODS@#The cerebral cortices of 1-day-old female rats were obtained and cultured for primary astrocytes. These cells were divided into 3 groups: control, lipopolysaccharide (LPS), and LPS+PR-957. The LPS group was treated with LPS (at a concentration of 5 μmol/L) for 48 hours; the LPS+PR-957 group was treated with PR-957 (at a final concentration of 200 nmol/L) for 1 hour and then LPS for 48 hours. Enzyme-linked immunosorbent assay was used to determine the expression of complement 3 (C3, a marker for A1 reactive astrocytes) and tumor necrosis factor alpha (TNF-α). Quantitative real-time PCR was used to determine the relative mRNA expression of glypican-6 (GPC6), SPARC-like 1 (SPARCL1), and lipocalin-2 (LCN2). All the above experiments were repeated three times independently.@*RESULTS@#C3 expression was almost not observed in the control group, but was observed in both the LPS group and the LPS+PR-957 group, with significantly lower expression observed in the LPS+PR-957 group (P<0.05). The expression of TNF-α was consistent with that of C3. Compared with the control group, the LPS and the PS+PR-957 groups had significantly reduced mRNA expression levels of GPC6 and SPARCL1 but significantly increased mRNA expression level of LCN2 (P<0.001). Compared with the LPS group, the LPS+PR-957 group had significantly increased mRNA expression levels of GPC6 and SPARCL1 but significantly reduced mRNA expression level of LCN2 (P<0.001).@*CONCLUSIONS@#LPS can induce the transformation from astrocytes to A1 reactive astrocytes, and PR-957 can inhibit the formation of LPS-induced A1 reactive astrocytes.

Increased expression of placenta growth factor in lung tissue of paraquat-induced rat pulmonary fibrosis model / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the dynamic expression of placenta growth factor (PLGF) in the lungs with paraquat (PQ)-induced pulmonary fibrosis.</p><p><b>METHODS</b>Forty-two adult healthy female Sprague-Dawley (SD) rats were randomly divided into two groups: the control group and the PQ group. Each group was divided into three subgroups, seven animals each. The rats in PQ group were treated intragastrically (ig) with PQ (40 mg/kg) and the rats in control group were treated with the same volume of saline at the beginning of the experiment. The animals of model and control group were sacrificed and lungs were harvested on the 7(th), 14(th) and 28th days respectively. A semiquantitative assay of histological examination and hydroxyproline in lung tissues were used to determine the severity of alveolitis and fibrosis. RT-PCR and immunohistochemistry were used to detect the mRNA and protein expression of PLGF.</p><p><b>RESULTS</b>Hydroxyproline contents in lung tissue were significantly increased after PQ administration. Inflammatory cell infiltration and fibrotic scores were more prominent in the model group compared to the control group. Further study showed that PLGF mRNA on day 7, 14 and 28 (1.28 +/- 0.29, 0.80 +/- 0.07, 0.65 +/- 0.13) and positive index of protein expression (2.27 +/- 0.34, 1.78 +/- 0.41, 1.25 +/- 0.69) in the PQ group were all upregulated as compared with those of the control group.</p><p><b>CONCLUSION</b>The PLGF expression in the lung tissue in rats with paraquat-induced pulmonary fibrosis is upregulated.</p>

Diagnostic value of ischemia-modified albumin in patients with acute coronary syndrome / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the diagnostic value of ischemia-modified albumin (IMA) for patients with acute coronary syndrome (ACS).</p><p><b>METHODS</b>We detected the IMA levels by albumin cobalt-binding (ACB) test and observed its dynamic changes in 492 patients with ACS, 74 patients with high blood pressure, 78 patients with viral myocarditis (VMC), 395 patients with acute chest pain (133 patients with acute ACS and 262 follow-up patients due to chest pain), 68 patients underwent percutaneous coronary intervention (PCI) and 830 healthy controls. Cardiac troponin I (cTnI) levels were assayed and electrocardiogram (ECG) recorded in patients with ACS.</p><p><b>RESULTS</b>The optimal diagnostic cutoff point for IMA in this study population was found to be 0.45 ABSU by ROC analysis. The IMA level (ABSU) in ACS group (0.55 +/- 0.11) was significantly higher than that in VMC group (0.38 +/- 0.11) and IMA levels in ACS and VMC groups were both higher than that in control and high blood pressure groups (0.34 +/- 0.08 and 0.35 +/- 0.08, all P < 0.05). IMA levels and the positive rates in patients with ACS were significantly higher (0.54 +/- 0.12 vs 0.44 +/- 0.12, 77.4% vs 39.3%, all P < 0.01) than those in chest pain follow-up group. In 133 patients with ACS, positive rate for IMA was significantly higher than that for cTnI within 1 h of admission (82.0% vs 40.6%, P < 0.01), and was similar at 6 - 24 h after admission (96.2% vs. 95.5%, P > 0.05). In 72 patients presenting to the emergency center within 3 h of acute chest pain and with negative cTnI, positive rate for IMA was 86.1% and for ECG 72.2%, the sensitivity for ACS diagnosis rised to 93.1% with both methods. The IMA leve was higher immediately after PCI than that before PCI (P < 0.05). IMA levels peaked 1d after hospitalization, then decreased gradually and returned to normal 14 days later.</p><p><b>CONCLUSIONS</b>IMA was a useful biochemical marker for the early diagnosis of ACS.</p>

Clinical on molecular basis of atrial fibrosis in patients with atrial fibrillation investigation / 中华心血管病杂志

<p><b>OBJECTIVE</b>To determine the molecular mechanisms involved in atrial fibrosis which occurs in patients with atrial fibrillation (AF) and to investigate their effects on the initiation and maintenance of AF.</p><p><b>METHODS</b>The right atrial tissue samples were taken from 73 patients with rheumatic heart disease who underwent heart valve replacement surgery. 34 patients had no history of AF (sinus rhythm group), 9 patients had paroxysmal AF and 30 patients had persistent AF. The mRNA content of collagen type I, collagen type III, MMP-2, TIMP-1, TIMP-2, TIMP-3 and TIMP-4 was measured by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and normalized to beta-actin or GAPDH.</p><p><b>RESULTS</b>Compared to sinus rhythm group, the mRNA of collagen type I and MMP-2 increased significantly in the persistent AF group (all, P < 0.01), followed by the paroxysmal AF group (all, P < 0.05). The mRNA of collagen type III was slightly higher in both AF groups than in the sinus rhythm group, but the differences were not statistically significant (P > 0.05). The mRNA of TIMP-1, TIMP-2 and TIMP-3 was down-regulated in the persistent AF group (all, P < 0.01, respectively), however, the trends of reduction did not reach statistical significance in the paroxysmal AF group (P > 0.05). The mRNA of TIMP-4 remained compatible in each group. The mRNA of collagen type I was significantly correlated with left atrial dimension (r = 0.336, P = 0.004) and AF duration (r = 0.339, P = 0.003). The mRNA of MMP-2 was significantly correlated with the mRNA of TIMP-2 (r = -0.326, P = 0.006), the mRNA of collagen type I (r = 0.322, P = 0.006), left atrial dimension (r = 0.300, P = 0.011) and AF duration (r = 0.300, P = 0.010).</p><p><b>CONCLUSION</b>The increased level of collagen type I associated with selective downregulation of TIMP-2 and upregulation of MMP-2 gene expression in atrium could be one of the molecular mechanisms of atrial fibrosis during atrial fibrillation, which correlates with the initiation and maintenance of AF.</p>

Changes in gelatinases expression and activity in human atria during atrial fibrillation / 中华心血管病杂志

<p><b>OBJECTIVE</b>To determine whether expression and activity of atrial gelatinases are altered in patients with atrial fibrillation (AF).</p><p><b>METHODS</b>The right atrial tissue samples were taken from 75 patients with rheumatic heart disease who underwent heart valve replacement surgery. 34 patients were in sinus rhythm, 11 patients had paroxysmal AF and 30 patients had persistent AF. The mRNA and protein level of MMP-2, MMP-9, TIMP-1, TIMP-2 were measured by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and Western-blotting analysis respectively. The activity of MMP-2 and MMP-9 was measured by zymographic analysis.</p><p><b>RESULTS</b>(1) The mRNA level of MMP-2 increased significantly in the persistent AF group followed by the paroxysmal AF group compared with the sinus rhythm group (P < 0.01, respectively). MMP-9 mRNA expression remained compatible within groups (P > 0.05). MMP-2 and MMP-9 protein expression was prominent in the persistent AF group compared with the sinus rhythm and paroxysmal AF groups (P < 0.01), the significant difference was also observed between the paroxysmal AF and sinus groups (P < 0.05). (2) TIMP-1 and TIMP-2 expression at mRNA and protein level were all down-regulated in the persistent AF group compared with the sinus rhythm group (P < 0.05), however, the trends of reduction did not reach statistical significance in the paroxysmal AF group (P > 0.05) except that of the mRNA level of TIMP-2 (P < 0.05). (3) The activity of MMP-2 and MMP-9 significantly increased in both paroxysmal AF and persistent AF groups compared with the sinus rhythm group (P < 0.05). The significant difference in MMP-9 was also observed between the persistent AF and paroxysmal AF groups (P < 0.01). (4) MMP-2 and MMP-9 expression at mRNA and protein level were positively correlated with left atrial dimension and AF duration (P < 0.05) and were negatively correlated with the mRNA and protein level of TIMP-2 and TIMP-1 respectively (P < 0.01).</p><p><b>CONCLUSIONS</b>The upregulation of MMP-2,9 gene expression and activity, along with the selective downregulation of TIMP-1,2 may have contributed to the atrial structural remodeling during AF through influencing collagen metabolism.</p>