[The molecular mechanism of apical hook development in dicot plant].

After the seeds of the dicot model plant Arabidopsis germinate in the soil, the tip of the hypocotyl will form a specialized structure called apical hooks to protect the cotyledons and shoot apical meristems from the mechanical damage during the soil emerging process. The development process of the apical hook is divided into three stages: the apical hook formation, maintenance, and opening. In recent decades, studies have shown that different kinds of plant hormones and environmental signals play a vital role in the development of the apical hook. As the downstream of a variety of signals, the asymmetric distribution of auxin and the signal transduction pathways play a decisive role in the development of the apical hook. However, the detailed mechanism of the asymmetric signal transduction pathway of the cells on both sides of the apical hook is still unclear. In this review, we summarize the molecular mechanisms of the development of apical hook and further refine the role of auxin in the development of apical hook, and prospect for future research directions in this field.

Antioxidative effect of luteolin pretreatment on simulated ischemia/reperfusion injury in cardiomyocyte and perfused rat heart.

OBJECTIVE: To investigate the antioxidative effect and mechanism of luteolin on rat cardiomyocytes and isolated hearts followed by simulated ischemia/reperfusion (SI/R) injury. METHODS: The left ventricular cardiomyocytes and the isolated hearts from adult rats were subjected to SI/R injury. The experiment groups included control, SI/R, luteolin + SI/R (Lut + SI/R), vitamin E (Vit E) + SI/R, and LY294002 + luteolin + SI/R (LY + Lut + SI/R) groups. Cell viability, shortening amplitude, lactate dehydrogenase (LDH) release, superoxide dismutase (SOD) activity, the production of reactive oxygen species (ROS) and malondialdehyde (MDA), expression levels of Akt, phosphorylated Akt, NOX2 (gp91phox), NOX2 mRNA, mitogen-activated protein kinase (p38 MAPK) and phosphorylated p38MAPK were all measured after 3-h simulated ischemia and 2-h simulated reperfusion procedure in cardiomyocytes. Vit E was used as a standard control. The contractile function of isolated hearts was further observed after they were subjected to 30-min global ischemia and 120-min reperfusion. RESULTS: Pretreatment with 8-µmol/L luteolin substantially increased cell viability and shortening amplitude, while reducing evidence of oxidative stress-induced damage in the cells. In addition, the expression of NOX2, NOX2 mRNA and phosphorylation of p38MAPK were all downregulated. Furthermore, pretreatment with 40-µmol/L luteolin improved the recovery of myocardial contractile function following SI/R-induced injury, and luteolin markedly increased phosphorylation of Akt. However, all of the above effects were partially inhibited by the phosphatidylinositol 3-kinase (PI3K) inhibitor, LY294002. CONCLUSIONS: Luteolin prevents SI/R-induced myocardial damage by reducing oxidative stress-induced injury in isolated rat hearts and cardiomyocytes, and the cardioprotection induced by luteolin was partially mediated by the PI3K/Akt pathway.

Luteolin Attenuates Foam Cell Formation and Apoptosis in Ox-LDL-Stimulated Macrophages by Enhancing Autophagy.

BACKGROUND: Our previous studies demonstrated that luteolin, which is rich in flavones, has various biological properties and can exert anti-oxidant, anti-inflammatory and anti-apoptotic activities. However, its effect on ox-LDL-induced macrophage lipid accumulation and apoptosis has not been revealed. AIMS: This study aimed to explore the role of luteolin in ox-LDL-induced macrophage-derived foam cell formation and apoptosis and to delineate the underlying mechanism. METHODS: Murine RAW264.7 cells were stimulated with oxidized low-density lipoprotein (ox-LDL) (50 µg/ml) for 24 h and then pretreated with 25 µM luteolin for another 24 h. The effects of luteolin on lipid accumulation in RAW264.7 cells induced by ox-LDL were assayed using Oil red O staining and high performance liquid chromatography (HPLC). Apoptosis was confirmed by acridine orange/ethidium bromide (AO/EB) staining, flow cytometric analysis and the TUNEL assay. Immunofluorescence, Western blot and monodansylcadaverine (MDC) staining analyses were then used to further investigate the molecular mechanisms by which luteolin protects macrophages from ox-LDL-induced foam cell formation and apoptosis. 3-Methyladenine (3-MA), an autophagy inhibitor, was used as a positive control. RESULTS: Treatment with 25 µM luteolin not only significantly attenuated ox-LDL-induced macrophage lipid accumulation but also decreased the apoptotic rate of RAW264.7 cells, the number of TUNEL-positive macrophages and the expression of Bax, Bak, cleaved caspase-9 and cleaved caspase-3. In addition, luteolin pretreatment significantly increased autophagosome formation and Beclin-1 activity, thus increasing the ratio of LC3-II/LC3-I. Moreover, these effects were abolished by 3-MA. CONCLUSIONS: Taken together, these results highlight that luteolin treatment attenuates foam cell formation and macrophage apoptosis by promoting autophagy and provide new insights into the molecular mechanism of luteolin and its therapeutic potential in the treatment of atherosclerosis.

Prevention of contrast-induced nephropathy with prostaglandin E1 in high-risk patients undergoing percutaneous coronary intervention.

PURPOSE: Contrast-induced nephropathy (CIN) is an important complication in the use of iodinated contrast media. The present study aimed to assess the safety and efficacy of prostaglandin E1 (PGE1) in prevention of CIN in patients with high-risk factors undergoing percutaneous coronary intervention (PCI). METHODS: The study group consisted of 163 patients who had undergone a coronary intervention procedure between January 1, 2012 and October 31, 2012. Study participants were randomly assigned to either the PGE1 group (82 patients) or the control group (81 patients). Patients in the PGE1 group received PGE1 intravenous infusion of 20 ng/kg/min for 6 h before and after the administration of contrast media. The control group received 0.9 % sodium chloride solution for routine hydration only. A nonionic, low-osmolality contrast agent was used in our laboratory at this time. Serum creatinine (Scr) values and estimated glomerular filtration rate were measured before and within 48 h of the administration of contrast agents. CIN was defined as an increase of ≥0.5 mg/dL or ≥ a 25 % increase in Scr concentrations over baseline within 48 h of angiography. RESULTS: The amount of contrast agent administered was similar for the PGE1 and control groups (156 ± 63 vs. 161 ± 68 mL, P > 0.05). The incidence of CIN was lower in the PGE1 group than in the control group (3.7 vs. 11.1 %, P < 0.05). No serious adverse effects were observed. CONCLUSIONS: In patients with high-risk factors undergoing PCI, the use of PGE1 for prevention of CIN is safe and efficacious.

The value of quantitative real-time myocardial contrast echocardiography for detection of angiographically significant coronary artery disease.

BACKGROUND: Real-time (RT) myocardial contrast echocardiography (MCE) is a novel method for the assessment of regional myocardial perfusion. We sought to evaluate the feasibility and diagnostic accuracy of quantitative RT-MCE in predicting significant coronary stenosis, with reference to quantitative coronary angiography. HYPOTHESIS: RT-MCE can identify anatomically significant coronary artery stenosis in selected patients. RT-MCE is probably an effective method for detection of angiographically significant coronary artery stenosis. METHODS: Thirty-five patients (mean age, 59.94 ± 10.63 years; 25 males) scheduled for coronary angiography underwent RT-MCE at rest, and shortly afterward underwent gated single-photon emission computed tomography (gated-SPECT). Coronary angiography was performed within 1 week after RT-MCE in all patients. The observing indexes included the images of RT-MCE that were analyzed quantitatively from microbubble replenishment curves for myocardial perfusion by using the Q-Lab software. The sensitivity and specificity of RT-MCE for quantitative detection of coronary artery disease (CAD) were obtained. The receiver operator characteristic (ROC) curves were used to assess the differences of accuracy in ischemic segments with A, ß and A × ß respectively. The sensitivity and specificity of gated-SPECT and RT-MCE for assessment of CAD were calculated using a 4-score method. RESULTS: A total of 513 segments among 595 segments in 35 patients were obtained. The cutoffs for A, ß and A × ß were 4.58, 0.64, and 2.73, and the sensitivity and specificity of quantitative RT-MCE for detection of CAD were 86.0%, 80.2%, 88.9%, and 84.1%, 64.6%, 79.9%, respectively. Meanwhile, the sensitivity and specificity of semiquantitative analysis for assessment of CAD were 66.7% and 61.8%. The ROC curve area of A and A × ß was 0.91 and 0.90 in the middle segments. The ROC area of A was 0.52 in the base segments. The sensitivity and specificity of gated-SPECT for assessment of CAD were 84.8% and 82.7%, respectively. The sensitivity of multi-indexes RT-MCE increased. The sensitivity was 89.1%, 90.4%, and 96.3% by A + ß, A + A × ß, and ß + A × ß. CONCLUSIONS: Quantitative RT-MCE is an effective method for the detection of coronary artery stenosis. Quantitative RT-MCE is segmented for assessment to ischemic myocardium. RT-MCE with multi-indexes has a valuable application for assessment of CAD surpassing SPECT.

Impact of anemia on contrast-induced nephropathy (CIN) in patients undergoing percutaneous coronary interventions.

BACKGROUND: The aim of the present study was to assess the influence of anemia on the risk of developing contrast-induced nephropathy after percutaneous coronary angioplasty. METHODS: Serum creatinine values were measured before and within 48 h after the administration of contrast agents. Contrast-induced nephropathy (CIN) was defined as an increase of ≥ 0.5 mg/dl or ≥ 25 % in serum creatinine concentration over baseline within 48 h after administration. Anemia was defined as hemoglobin <120 g/l in women and <130 g/l in men. RESULTS: Among the 1,026 patients studied, 32 (3.1 %) developed CIN after procedure. CIN occurred in 6.3 % of the anemic patients and in 2.2 % of the non-anemic patients (P < 0.01). The incidence of CIN increased with decreasing of baseline estimated glomerular filtration rate (eGFR) in both the anemia and non-anemia groups. In patients with baseline eGFR <30 ml/min, a high proportion of both anemic and non-anemic patients experienced CIN (24.6 vs. 17.5 %). When baseline eGFR was 30-59 ml/min, the incidence of CIN in anemic patients was twofold higher than in non-anemic patients (7.9 vs. 3.8 %; P < 0.05). Multivariate logistic regression analysis found that baseline eGFR and baseline hemoglobin were independent predictors of CIN. CONCLUSION: Anemia is associated with a higher incidence of CIN in patients with moderate renal dysfunction. Patients with both preexisting renal insufficiency and anemia are at high risk of CIN. Baseline eGFR and baseline hemoglobin are independent predictors of CIN.

Real-time three-dimensional echocardiographic evaluation of left ventricular systolic synchronicity in patients with chronic heart failure: comparison with tissue Doppler imaging.

BACKGROUND: To investigate the clinical value of real-time three-dimensional echocardiography (RT-3DE) for assessing of left ventricular systolic synchronicity. METHODS: Thirty healthy volunteers and 62 patients with congestive heart failure (CHF) were enrolled. The SD of time to peak systolic motion (TDI-Ts12-SD) was measured with tissue Doppler imaging in 12 myocardial segments. The SD and maximal difference of the time to minimal systolic volume (Tmsv) between 16, 12, or 6 myocardial segments, expressed as a percentage of cardiac cycle duration, were measured with RT-3DE and labeled Tmsv16-SD%, Tmsv12-SD%, Tmsv6-SD%, Tmsv16-D%, Tmsv12-D%, and Tmsv6-D%, respectively. The Spearman coefficient and Kappa value were calculated, and Bland-Altman analysis was performed to investigate the correlation and agreement between the two methods. Tmsv values were compared with ejection fraction (EF). RESULTS: There was a moderately positive (p< 0.01) correlation between TDI-Ts12-SD and Tmsv16-SD%, Tmsv12-SD%, Tmsv16-D%, and Tmsv12-D% (r = 0.65, 0.64, and 0.65, respectively, with Kappa values of 0.66, 0.65, 0.72, and 0.74, respectively, p< 0.01). Tmsv16-SD%, Tmsv12-SD%, and Tmsv12-D% were significantly different between CHF patients with EF ≤ 35% and those with EF > 35%. CONCLUSIONS: RT-3DE can be used in patients with CHF to quantify left ventricular mechanical dyssynchrony. Tmsv12-SD% and Tmsv12-D% were the best indices of left ventricular systolic synchronicity in relation to the severity of CHF as evaluated from EF.

Clinical usefulness of low-dose dobutamine stress real-time myocardial contrast echocardiography for detection of viable myocardium.

OBJECTIVES: To evaluate and compare the diagnostic accuracy of semi-quantitative and quantitative real-time myocardial contrast echocardiography (RT-MCE) with low-dose dobutamine stress echocardiography (LD-DSE) in detecting viable myocardium. METHODS: Thirty in-patients with coronary artery disease and regional wall motion abnormalities underwent RT-MCE without and with LD-DSE. Percutaneous coronary intervention was performed within 1 week after RT-MCE in all patients. Myocardial perfusion was evaluated from A, ß, and A × ß indices from microbubble replenishment curves. The motion of each myocardium segment was observed by routine echocardiography 1, 3, and 6 months after percutaneous coronary intervention and its improvement over time was the criterion of viable myocardium. RESULTS: RT-MCE sensitivity and specificity for the assessment of viable myocardium were 71.7% and 69.8%, rising to 81.3% and 76.7% (p < 0.05) when combined with LD-DSE. Using quantitative RT-MCE with cutoff values of A, ß, and A × ß, the sensitivity and specificity were 75.6%, 78.8%, 82.1%, and 82.4%, 77.9%, 78.6%, respectively. When combined with LD-DSE, the sensitivity and specificity were 86.0%, 83.2%; 88.9% and 84.1%; 89.6%, 79.9%, respectively. CONCLUSIONS: Quantitative RT-MCE analysis yielded higher sensitivity and specificity than semi-quantitative RT-MCE with or without LD-DSE for the detection of viable myocardium.

Salvianolic acid A inhibits angiotensin II-induced proliferation of human umbilical vein endothelial cells by attenuating the production of ROS.

AIM: To investigate the action of salvianolic acid A (SalA) on angiotensin II (Ang II)-induced proliferation of human umbilical vein endothelial cells (HUVECs) and the possible signaling pathways mediating this action. METHODS: Cell proliferation was examined with MTT assay. The expression levels of Src phosphorylation (phospho-Src), Akt phosphorylation (phospho-Akt), and NADPH oxidase 4 (Nox4) in HUVECs were determined by Western blot. The production of reactive oxygen species (ROS) was estimated using fluorescence-activated cell sorting (FACS). RESULTS: SalA (6.25-50 µmol/L) did not affect the viability of HUVECs. Treatment of HUVECs with Ang II (1 µmol/L) markedly increased the cell viability; pretreatment of HUVECs with SalA (12.5, 25 and 50 µmol/L) prevented Ang II-induced increase of the cell viability in a concentration-dependent manner. Treatment of HUVECs with Ang II (1 µmol/L) markedly up-regulated the protein expression levels of phospho-Src, phospho-Akt (473) and Nox4; pretreatment of HUVECs with SalA (12.5, 25 and 50 µmol/L) blocked all the effects in a concentration-dependent manner. Treatment of HUVECs with Ang II (1 µmol/L) dramatically increased ROS production in HUVECs; pretreatment of HUVECs with SalA (12.5, 25 and 50 µmol/L) blocked the ROS production in a concentration-dependent manner. CONCLUSION: SalA inhibits Ang II-induced proliferation of HUVECs via reducing the expression levels of phospho-Src and phospho-Akt (473), thereby attenuating the production of ROS.