Curcumin is a principal polyphenolic curcuminoid extracted from turmeric rhizome, which has been used for treating inflammation of joints, ulcers, jaundice and other disorders in Asian traditional medicine. In recent years, many studies have indicated that curcumin plays important roles in treatment of liver diseases. Curcumin attenuates liver injury and non-alcoholic fatty liver disease by lowering the release of inflammation cytokines, minimizing oxidative stress, enhancing the sensitivity of insulin and altering lipid metabolism. Curcumin shows potent anti-fibrosis activity, contributing to inhibit the activation of hepatic stellate cells and reduce the deposition of extracellular matrix by its regulation of PPAR-γ, NF-ΚB and TGF-β signaling pathways. Moreover, curcumin exhibits anti-cancer effect by inducing G2/M phase cell cycle arrest and apoptosis in several hepatoma cell lines. However, poor water solubility and low bioavailability of curcumin limit its clinical applications. To overcome its limited systemic bioavailability, many new approaches have been explored to deliver curcumin effectively. This article focuses on advances in the effects of curcumin and its derivatives for treatment of liver injury, non-alcoholic fatty liver disease, liver fibrosis and hepatocarcinoma.

Objective To investigate the influence of blood pressure level on carotid intima‐media thickness (CIM T ) and plaque in elderly patients with coronary heart disease(CHD) .Methods 100 elderly CHD patients with hypertension admitted in our hospital from Jan .to Dec .2012 was collected .an epidemiological investigation was applied ,and blood pressure was measured .carotid CIMT and plaque were determined by colored Doppler ultrasound .multivariate linear regression model or Logistic regression model was used to analyze the effect of blood pressure on CIMT and plaque .Results A total of 100 subjects were enrolled .CIMT and plaque prevalence were (0 .7 ± 0 .1)mm ,45 .8% in 48 males and (0 .7 ± 0 .1)mm ,34 .6% in 52 females .the difference was statisti‐cally significant(χ2 =5 .609 ,P=0 .018) .multiple regression models showed that ,after adjusting relevant factors ,CIMT increased 0 .001 14 mm with SBP 1 mm Hg increase and CIMT increased 0 .001 18 mm with pulse pressure 1 mm Hg increase in males .Lo‐gistic regression model showed that the risk of plaque number >1 was higher in grade Ⅲhypertension compared to grade 1 hyper‐tension(OR= 2 .115 ,95% CI= 1 .128~ 3 .966 ,P= 0 .020) .Conclusion Elderly CHD patients with hypertension ,especially in males ,carotid CIMT increase while systolic BP and high pulse are high ,which cause the high risk of carotid artery plaque;hyperten‐sion is a independent risk factor for atherosclerosis in elderly CHD patients .

Objective To investigate the effects of valsartan on experimental left cardiac function and the vasoactive substance in rats with acute myocardial infarction (AMI).Methods Seventy Wistar rats were randomly divided into 6 group:①Sham groups: including Sham 1(n=5) and Sham 4(n=5).The pericardium of rats in Sham groups were cut open and sutured immediately.The rats were routinely breeded for 1 week and 4 weeks,1.5 mL saline was poured into stomach once a day.②Control groups: AMI 1 (n=10) and AMI 4 (n=10).Anterior descending branches of coronary artery of Wistar rats were ligated to establish models of AMI.The rats with AMI were poured into stomach with 1.5 mL saline once a day after AMI for 1 week and 4 weeks.③Valsartan groups: VAS 1 (n=10) and VAS 4 (n=10).The rats with AMI were poured into stomach with valsartan 10 mg?kg-1 and 1.5 mL saline for 1 week and 4 weeks(once a day).Cardiac function was assayed by arterial cannulatio.Angiotensin Ⅱ(Ang Ⅱ),aldosterone (ALD),endothelin (ET),thromboxane A2(TXA2) and prostacyclin I2 (PGI2) in serum were measured by radioimmunoassay.Results ① Valsartan could evidently improve cardiac function on the 1st and 4th week after experimental AMI.+dp/dtmax and-dp/dtmax were both increased on the 1st and 4th week and more evidently on the 4 week.②Compared with control groups,valsartan decreased the levels of ALD,ET and TXA2 in plasma and increased the levels of AngⅡ and PGI2 in plasma.Conclusion Valsartan could improve left cardiac function on late stage of infarction,the effect improve not only systolic function,but also diastolic function.

Objective:We estimated the effect of Xinxuetong on the left ventricular function in hyperten-sion. Methods :Transaortic and transmitral flow velocity was studied by pulsed Doppler echo cardiographybefore and after vein administration of Xinxuetong. Results: It was shown that Peak A, IRP andPeak A/Peak E decreased after administration of Xinxuetong. Conclusion:This study suggests that Xinx-uetong can significantly improve the diastolic function and the treatment of hypertension.

Objective The enhanced patterns of atherosclerotic plaque on dynamic contrastenhanced MRI have not been well studied. The aim of this study was to explore the patterns of plaque enhancement and their underlying mechanism by using dynamic contrast-enhanced MRI (DCE-MRI).Methods Atherosclerotic plaques were induced in the aorta of 12 New Zealand White rabbits by a combination of endothelial denudation and high-cholesterol diet. Ten to sixteen weeks after surgery, DCEMRI was performed with a fast spin echo T1 weighted sequence. Thirty-five phases of images were obtained at 71-second intervals. Gd-DTPA was injected coincident with the third scan via marginal ear vein. Specimens were harvested within 12 hours after imaging for HE staining and CD31 immunohistochemical staining which was used to highlight nco-vessels. Plaque enhancement patterns were studied and compared with histological findings. Signal intensity of each plaque section was normalized to pre-contrast signal intensity of psoas muscle, after which signal intensity versus time curve was drawn. Pearson correlation coefficient was used to reveal association between histological neo-vessel count and descriptive parameters derived from signal intensity versus time curve. Results Plaques were significantly enhanced by Gd-DTPA. Enhancement patterns could be described as fast-in and slow-out. Differences in patterns of enhancement were observed between tissues, with fibrous tissue enhanced more than lipid aggregation and leukocyte foci. Peak enhancement( 1. 05 ±0. 30) , initial slope(0. 82 ± 0. 28 ) and area under the curve at early phase(4.97 ± 1.67) derived from signal intensity-time curve had significant correlations with neo-vessel count( 117.7 ± 93. 3) ( r= 0. 553,0. 468, 0. 554 respectively, P ＜ 0. 05 ) . Conclusions The enhanced patterns of atherosclerotic plaque by Gd-DTPA were fast- in and slow-out. Neovascularization, increased endothelial permeability and extracellular matrix may be the reasons for plaque enhancement by Gd-DTPA. DCE-MRI has the potential to quantify the extent of neo-vasculature formation within plaques.

Objective To investigate the relationship between microalbuminuria (MAU) and the risk factor for acute ischemic stroke,the severity of the disease and outcomes.Methods A total of 156 consecutive patients with acute ischemic stroke were enrolled prospectively.They were randomly divided into either an MAU positive group (≥ 30 mg/g) or an MAU negative group (＜ 30 mg/g) according to urinary albumin/creatinine ratio (UACR).They were also randomly divided into either a good outcome group (0-2) or a poor outcome group (＞2) according to the modified Rankin scale (mRS) scores.The various demographic and clinical data were compared,and the poor outcome of acute ischemic stroke and the independent factors of positive MAU were analyzes.Results A total of 156 patients with acute ischemic stroke were enrolled,including 84 males and 72 female; aged 53 to 78 years (mean 65.4 ± 6.2); the time from onset to admission was 1.5 to 28 h; 94 patients had good outcomes,62 had poor outcomes,and no one died; MAU was positive in 76 patients and MAU was negative in 80 ones.Multivariate logistic regression analysis showed that advanced age (odds ratio [OR] 1.992,95％ confidence interval [CI] 1.108-2.374; P =0.015),complicated with diabetes (OR 2.497,95％ CI 1.177-5.298; P =0.017) and atrial fibrilhtion (OR 2.338,95％ CI 1.062-5.148; P =0.035),high serum homocysteine (Hcy) level (OR 2.541,95％ CI 1.073-6.02; P =0.047) and UACR (OR 2.130,95％ CI 1.396-3.017; P =0.001),MAU positive (OR 3.291,95％ CI 1.681-6.444; P =0.001),high baseline National Institutes of Health Stroke Scale (NIHSS) score (OR 9.196,95％ CI 2.828-19.815; P＜ 0.001) were the independent risk factors for poor outcomes in patients with acute ischemic stroke.There were significant differences in the proportion of the patients complicated with diabetes (P =0.038) and fasting blood glucose level (P =0.025),serum Hey level (P =0.022),and carotid intima-media thickness (IMT) (P =0.019) between the MAU positive group and the MAU negative group.The proportion of anterior circulation infarction was lower (P =0.033),the rates of the baseline NIHSS score (P =0.003) and poor outcome were higher in the MAU positive group (P ＜ 0.001).Multivariate logistic regression analysis showed that increased diabetes (OR 2.237,95％ CI 1.036-4.829; P =0.040) and fasting blood glucose (OR 1.223,95％ CI 1.145-1.673; P =0.027),the increased Hey level (OR 2.542,95％ CI 1.047-6.612; P=0.025),carotid artery IMT (OR 1.295,95％ CI 1.106-1.362; P =0.023) and baseline NIHSS score (OR1.206,95％ CI 1.044-1.219; P =0.023) were correlated independently with the positive MAU in patients with acute ischemic stroke.Conclusions Positive MAU is one of the independent risk factors for poor outcomes of acute ischemic stroke,it is closely associated with some risk factors for acute ischemic stroke,and it has a significant impact on the severity of acute ischemic stroke and outcomes.

Objective To evaluate the protective effect of Ulinastatin on pathological changes of lung induced by paraquat (PQ) intoxication in rats. Method Sixty female SD rats were randomly and equally divided into three groups ( n = 20 in each group). On the experimental day, the rats of group A (control group) received 1 mL of saline intragastrically; the rats of group B (PQ, group) received 1 mL of PQ intragastrically (40 mg/kg diluted in saline) and then treated with saline injected intraperitoneally once a day, and the rats of group Group C (Ulinastatin treatment group) received 1 mL of PQ intragastrically (40 mg/kg,diluted in saline) and then treated with 1 mL of Ulinastatin ( 120 000 IU/kg) intraperitoneally twice a day. The rats ( n = 5 in each subgroup) were sacrificed on the 7th, 14th, 21st, and 28th day for observing the histopathological changes of the lung stained with hematoxylin-eosin stain (HE) and Masson's trichrome stain. Data were semi-quantitatively analyzed by SPSS10.0 software. Hierarchical data were analyzed by rank and inspection. The data that have significance analyzed by comparison test (Bonferroni methods). Results Paraquat intoxication resulted in significant alveolitis and lung fibrosis. Ulinastatin treatment alleviated lung edema, hemorrhage, inflammatory cell infiltration, and fiber aggregation. Conclusions These data demonstrated the Ulinastatin exerted protective effects against PQ-induced lung injury. Ulinastatin could to be used in clinical management for PQ intoxication.

Objective To explore the diagnostic value of NAP activity detection in SLE.Methods Technique of AS-BI was used to NAP staining of peripheral blood smear in patients with newly-diagnosed SLE(30 cases)and normal healthy women(30 cases),to observe positive rate and positive score of NAP.Results The positive rate was(22.1±8.8)% in group SLE,(56.8±9.4)% in group normal;The positive score was(22.2±8.9)in group SLE,(58.2±9.8)in group normal.The positive rate and positive score were much lower in patients with SLE comparing with those in group normal.Differences were statistically significant(P＜0.01).Conclusions The detection of NAP is useful in the patients with newly-diagnosed SLE,but we must go on researching the pathogenesis of NAP activity decreased in SLE.

Objective To investigate the effect of selective phosphatase inhibitors Salubrinal on autophagy and apoptosis in the lung tissue of rats with acute paraquat (PQ) poisoning,and to explore its mechanism.Methods 200 Wistar rats were randomly divided into four groups by randomized arrangement table formed by computer,with 50 rats in each group.PQ poisoning model was reproduced by one time gastric lavage with 1 mL of 40 mg/kg PQ solution followed by intraperitoneal injection of 1 mL normal saline (NS) once a day.The rats in control group were lavaged once with 1 mL of NS followed by intraperitoneal injection of 1 mL NS twice a day.The rats in Sal 0.5 and Sal 1.0 groups were intraperitoneal injected with 1 mL Salubrinal 0.5 mg/kg or 1.0 mg/kg on the 1st,3rd,and 5th day after PQ poisoning once a day.The lung tissue was harvested on the 7th day after poisoning,and the changes in histomorphology were observed using hematoxylin and eosin (HE) staining.The positive expression of autophagy-related protein LC3-Ⅱ in lung tissue was observed after immunohistochemistry staining,and LC3-Ⅱ and caspase-3 protein expressions were determined by Western Blot.Results HE staining results showed partial abnormal pulmonary structure in the PQ poisoning group:collapse of pulmonary alveoli,enlargement of the cavity,local infiltration of inflammatory cells,increasing thickness in the alveoli wall and obvious bleeding in the local lung tissue.Compared with the PQ poisoning group,the above changes in Sal 0.5 and Sal 1.0 groups were obviously relieved.It was shown by immunohistochemistry staining that compared with control group,the positive expression of LC3-Ⅱ was obviously decreased in the PQ poisoning group,Sal 0.5,and Sal 1.0 groups (A value:78.34 ± 10.71,76.52 ± 8.21,77.48 ± 9.11 vs.117.58 ± 15.26,all P＜0.05).There was no significant difference in positive expression of LC3-Ⅱ between each of the later three groups (all P＞0.05).Western Blot results showed:compared with the control group,the protein expressions of LC3-Ⅱ and caspase-3 were significantly increased in PQ poisoning group [LC3-Ⅱ (A value):0.22 ±0.05 vs.0.14 ±0.03,caspase-3 (A value):0.115 ± 0.013 vs.0.023 ± 0.006,both P＜0.05].Compared with PQ poisoning group,the protein expressions of LC3-Ⅱ and caspase-3 were obviously decreased in the Sal 0.5 and Sal 1.0 groups [LC3-Ⅱ (A value):0.19 ±0.05,0.18 ±0.04 vs.0.22 ±0.05; caspase-3 (A value):0.078 ±0.012,0.076 ±0.010 vs.0.115 ±0.013,all P＜0.05].Conclusions The endoplasmic reticulum stress-autophagy is activated in the pulmonary cell of acute PQ poisoning rats.Salubrinal can decrease the autophagy and apoptosis in the lung of rats with acute PQ poisoning,which play a role in the treatment.

Objective To investigate the effects of ulinastatin on autophagy and apoptosis of lung cells in rats with acute paraquat poisoning.Methods A total of 150 Wistar rats were randomly (random number) divided into three groups.The rats in control group had stomach lavaged once with 1 mL of normal saline followed by intraperitoneal injection of 1 mL normal saline twice a day.PQ poisoning model was produced by stomach lavaged once with 1 mL of 40 mg/kg PQ solution followed by intraperitoneal injection of 1 mL normal saline once a day.In PQ + ulinastatin (PU) group,UTI in dose of 12 000 U/kg was intraperitoneally injected in rats twice a day.The lung tissue was obtained on the 7th day after modeling,and the histopathological changes were observed under microscope after hematoxylin and eosin (HE) staining.The positive expressions of autophagy-related LC3 protein LC3 and Bcl-2 pretein in lung tissue were observed after immunohistochemistry staining,and the levels of LC3、Bax 、Bcl-2 proteins were determined by Western blot.Results HE staining Results showed:it was observed from the PQ poisoning group that the abnormal cellular structure,enlargement in the pulmonary alveoli,leaking a lot of inflammatory cells,increased thickness of the alveoli wall and bleeding in the local area of lung tissue.Compared with the PQ poisoning group,the above changes in ulinastatin groups were relieved.Western blot Results showed:compared with the control group,the protein expressions of LC3-A/B were significantly increased in PQ poisoning group [LC3-A/B expression (A scale):0.22 ± 0.05 vs.0.14 ± 0.03,F =22.48,P ＜ 0.01].compared with PQ group,the expression of LC3 A/B obviously increased in the group of PU [LC3-A/B expression (A scale):0.36 ± 0.08 vs.0.22 ± 0.05,F =22.78,P ＜ 0.01].compared with Con group,the expression of Bcl-2/Bax obviously decreased in the group of PQ [Bcl-2/Bax expression (A scale),0.11 ±0.04 vs.0.83 ± 0.09,F =154.43,P ＜ 0.01].Compared with PQ poisoning group,the protein expressions of Bcl-2/Bax were obviously increased in PU groups [Bcl-2/Bax expression (A scale):(0.63 ± 018) vs.(0.11 ±0.04),F =154.43,P ＜0.01].Immunohistochemistry result:compared with Con group,the expression of LC3 and Bcl-2 obviously decreased in the group of PQ [LC3expression (A scale):(78.34±10.71) vs.(117.58±15.26),F=31.63,P＜0.01) (Bcl-2 expression (A scale):(62.54±9.74)vs.(130.52 ± 9.86,F =118.44,P ＜ 0.01).Compared with PQ poisoning group,the protein expressions of LC3 and Bcl-2 were obviously increased in PU groups [LC3expression (A scale):(162.58 ± 25.76) vs.(78.34 ± 10.71),F=31.63,P＜0.01]; [Bcl-2 expression (A scale):(145.56±10.26) vs.(62.54±9.74),F=118.44,P ＜ 0.01].Conclusions Theendoplasmic reticulum stress-autophagy is activated in the lung cells of rats with acute PQ poisoning.UTI can adjust endoplasmic reticul um stress,increased the expression of Bcl-2 and enhance the proportion of Bcl-2/Bax to protect the lungs of rats from acute PQ poisoning.