AIM To investigate if the protective effect of baicalin on cerebral injury induced by transient focal ischemia is related to modulation of expressions of inflammatory cytokines or adhesive molecules. METHODS Transient focal cerebral ischemia injury model in rats was induced by occlusion of the right middle cerebral artery for 2 h, followed by 24 h reperfusion. The infarct volume and neurological deficit were determined by TTC staining and the scoring method of Longa et al. The expression of intracellular adhesion molecule-1 (ICAM-1), neutrophils infiltration, and myeloperoxidase (MPO) activity in brain were measured by immunohistochemistry, hematoxylin-eosin staining, and spectrophotometer, respectively. Semiquantitative RT-PCR was employed to assess the expression of inducible nitric oxide synthase (iNOS) mRNA. The level of interleukin-1 (IL-1) in brain was assayed by radioimmunoassay. The expression of nuclear factor-κB (NF-κB) protein was evaluated by Western blot. RESULTS After transient cerebral ischemia, MPO activity and the expression of ICAM-1 in the periphery of ischemic cortex were significantly increased. Increase in iNOS mRNA and NF-κB protein expression was also shown in the ischemic area. Treatment with baicalin markedly reduced brain infarct volume and neurological deficit induced by ischemic insult, inhibited MPO activity, inflammatory cell infiltration, as well as expression of ICAM-1, iNOS and NF-κB, and decreased IL-1 level. CONCLUSION Baicalin may play a protective effect on cerebral ischemic injury through inhibiting the expression and release of the inflammatory mediators after cerebral ischemia.

AIM: To study the protective effects of baicalin on myocardial ischemia-reperfusion injury in rats. METHODS: The models of myocardial ischemia-reperfusion injury were established by occluding left anterior descending coronary artery (LAD) for 30 min, followed by reperfusion for 120 min. The rate of rise and decline of left ventricular pressure (±dp/dtmax) and end-diastolic pressure of left ventricle (LVEDP) were monitored continuously with polygraph. After reperfusion, the blood and myocardium samples were taken for determination of malondialdehyde (MDA) content, superoxide dismutase (SOD), Na+-K+-ATPase, Ca2+-ATPase activities in myocardium, creatine kinase (CK) and lactate dehydrogenase (LDH) in serum with spectrophotometer. The ultrastructural changes in ischemic myocardium were assessed by transmission electron microscope. RESULTS:dtmax and LVEDP, decreased plasma CK and LDH levels, reduced myocardial MDA content, and increased the activities of SOD, Na+-K+-ATPase, and Ca2+-ATPase in myocardium following ischemia-reperfusion. The ultrastructural injury in reperfused myocardium was relieved. CONCLUSION: Baicalin possesses a protective effect against myocardial ischnemia-reperfusion injury through scavenging oxide radicals and improving Na+-K+-ATPase and Ca2+-ATPase activities.

Objective:To study the effect of diammonium glycyrrhizinate (DG) on left ventricular function impairment during myocardial ischemia－reperfusion in rats.　Methods:The left ventricular was cannulated through right common carotid artery on the myocardial ischemia－reperfusion injury model. The left ventricler function was assessed before and 10 minutes after the administration of DG, immediate and 20 minutes after initiation of ischemia, immediate and 30, 60 minutes after reperfusion, by measuring the left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP), ＋dp*dtmax and －dp*dtmax. 　Results:Compared with the baseline, all measurements of LVSP, ＋dp*dtmax and －dp*dtmax decreased (P＜0.05,P＜0.01), while LVEDP increased (P＜0.01) after administration of DG. As the time of ischemia－reperfusion lasting, LVSP, dp*dtmax and －dp*dtmax generally decreased progressively, while LVEDP generally increased progressively. 20 minutes after the initiation of ischemia and immediate, 30 and 60 minutes following reperfusion, LVSP, ＋dp*dtmax and －dp*dtmax in the DG group were significantly higher than those in IR group (P＜0.01), LVEDP significantly lower than that in IR group (P＜0.01) at the same time. 　Conclusion:DG can protect left ventricular function against myocardial ischemia－reperfusion injury in rats.

Aim To explore the role of endoplasmic reticulum stress (EPR) in high fatty acid induced injury in cardiomyocytes.Methods Cardiomyocytes were exposed to different concentrations of palmitic acid (0, 0.1, 0.2, 0.4 mmol·L-1) for 24 h and different time points of high palmitic acid (0.2 mmol·L-1) (12, 24, 48 h).Cell viability was measured by CCK8, and the protein expressions of EPR such as GRP78, CHOP, PERKphos, IRE1phos, ATF6 and apoptosis related proteins such as Bcl-2 and Bax were determined by Western blot.Results When the cells were stimulated with palmitic acid (0.1~0.4 mmol·L-1) for 24 h, the cell proliferation rates of 0.2 and 0.4 mmol·L-1 groups were significantly decreased.Cardiomyocytes exposured to high palmitic acid (0.2 mmol·L-1) for 24 h showed an increase in theexpression of EPR related proteins (GRP78, CHOP, PERKphos, IRE1phos and ATF6) and Bax(P<0.05), while Bcl-2 expression was significantly reduced.Pretreatmented with EPR inhibitor pravastatin(10 mol·L-1) significantly increased high palmitic acid induced Bcl-2 expression (P<0.05) and significantly decreased high palmitic acid induced Bax expression (P<0.05).Conclusion Activated EPR might play an important role in treatment of high fatty acid induced myocardial injury.

Objective To discuss the application value of texture analysis of conventional MRI in differential diagnosis of orbital lymphoma from inflammatory pseudotumor.Methods The conventional MRI data of 15 patients with lymphoma and 17 patients with inflammatory pseudotumor proven by pathology or clinical follow-up were retrospectively reviewed.The texture features of lesions based on axial T1WI,fat-saturated T2WI and contrast enhanced fat-saturated T1WI were extracted by manually drawn ROIs with software MaZda.The subsets of optimized texture parameters were chosen by four different methods:Fisher coefficient,probability of classification error and average correlation coefficient (POE+ ACC),mutual information measure (MI) and the combination of the above three methods (FPM),respectively.Linear discriminant analysis (LDA) and nonlinear discriminant analysis (NDA) were performed for texture classification.The texture features from the sequence with the best classification result of orbital lymphoma and inflammatory pseudotumor were compared.Results The optimal texture parameters were mainly derived from co occurrence matrix and run-length matrix on T1WI and T2WI.The optimal texture parameters were mainly derived from co-occurrence matrix and histogram on contrast enhanced T1WI.The best classification of MRI texture was obtained within T2WI with lowest classification error of 1.56％ achieved by FPM in combination with NDA.Comparing the texture parameters of orbital lymphoma and inflammatory pseudotumor on T2WI,the angular second moment and long length emphasis were significantly higher in orbital lymphoma (both P＜0.005),while the entropy and short length emphasis were significantly lower in orbital lymphoma (both P＜0.005).Conclusion It is feasible to use texture analysis on conventional MRI for the differentiation of orbital lymphoma and inflammatory pseudotumor.

Aim To investigate the relationship between oxidative stress and the aortic endothelial cells injury in type 2 diabetes rats,as well as the effect of valsartan. Methods The type 2 diabetic models were induced by low dose of streptozotocin (STZ) with high-energy diet.12 weeks after injecting STZ, rats were randomly divided into three groups: normal control, diabetes control and valsartan (24 mg?kg-1?d-1, 8 weeks, ig.) treated diabetes. At the 12th and 20thweek end, such indices as the endothelium-dependent vasodilation and the shape of aorta endothelium, the serum contents of SOD, GSH-Px , MDA and NO, and the level of NOS gene expression in aorta were measured. Results ① At the 12th weekend,in the diabetes group, the relaxation of aortic rings to low concentration of Ach declined, the aortic endothelial cells intumesced, contents of serum SOD, GSH-Px, MDA and NO significantly increased, the expression of iNOS mRNA in aorta obviously up-regulated while the expression of eNOS mRNA showed no change. ② At the 20th weekend,in the diabetes control group, the dilatory reactivity of aortic rings decreased to each concentration of Ach, the aortic endothelium appeared degenerative and necrotic, activities of SOD and GSH-Px decreased as well as the content of NO, the content of MDA increased continuously, and the iNOS mRNA expression up-regulated while eNOSmRNA expression down-regulated. Valsartan could regress the aggravation and improve contents of serum SOD, GSH-Px, MDA, NO and NOS mRNA of the aorta. Conclusion The oxidative stress and abnormality of NO participate the process of aortic endothelial cell injury. Valsartan plays a protective role partially through enhancing antioxidation effect and adjusting NO production.

Aim To study the inhibitory effects and its mechanis ms of Garlic Polysaccharide (GP) on adriamycin(ADR)-induced cardiotoxicity in mic e.Mehtod ADR was injected intraperitoneally to induce myocardiu m injury model in mice. The activities of several serum and heart tissue enzymes were measured. With scanning electron microscope, the cardiac ultrastructural c hanges were examined.Results ADR (3 mg?kg -1 ip, qod?7) induced severe myocardial damages with the increasing activities of creatine kin ase (CK), lactate dehydrogenase (LDH), glutamic oxaloacetic transaminase (GOT) a nd inducible nitric oxide synthase (iNOS) (P

IHC-65 was found to be a potent inhibitor of platelet function . It inhibited platelet aggregation induced by threshold concentration of ADP, arachidonic acid and collagen with dose-dependent manner in vitro, and at 96?mol/L, AIR ( aggregation inhibition rate,) were 71.56, 66.93 and 68.47% respectively. IHC-65 inhibited platelet serotonin release induced by collagen,and at 96 ?mol/L, release inhibition rate was 82.97%. IHC-65 did not influence cAMP level in platelet significantly. It is concluded that IHC-65 inhibited platelet aggregation and its action mechanism may be related to inhibition of serotonin release and to antagonizing Ca ++ .

Aim To explore the effects of lipoteichoic acid (LTA) induced delayed preconditioning (PC) on hypoxia-reoxygenation (H/R) injury of cultured human coronary artery endothelial cells (HCAECs), and to investigate the potential role of endogenous nitric oxide (NO) participated in the protective mechanism. Methods HCAECs were incubated for 2 h in a hypoxic atmosphere and reoxygenated for 4 h in a normoxic atmosphere. The delayed PC was induced by pretreatment with LTA assessed by the percentage of cellular injury with Trypan blue exclusion and by the amount of lactate dehydrogenase (LDH) in culture media. The NO level of the culture media was measured detect the expression of eNOS mRNA by RT-PCR method after cells were recovered from different points.Results LTA pretreatment significantly decreased the percentage of the killed cell and the concentration of LDH in media. Also, LTA pretreatment obviously raised the concentrations of NO in culture media. The protective effects of LTA were abrogated by pretreatment with N-monomethyl-L-arginine (L-NMMA).Moreover, the expression of eNOS mRNA was significantly upregulated after HCAECs exposure to LTA for 4 h following 2 h or 4 h recovery. Conclusion LTA could induce the delayed protection against H/R induced endothelial injury and dysfunction of cultured HCAECs. NO produced by eNOS acts initially as a trigger and subsequently as a mediator of delayed PC.

Objective: To study the protective effects of tetrahydropalmatine (THP) against ischemia－reperfusion induced hippocamp lesion in rats. 　MethodS: A model of ischemia-reperfusion induced brain lesion was set up by ligation of common carotid arteria in rats, and the protective effects of THP was observed.　Results: It was found that, with administration of THP, the activities of superoxide dismutase (SOD), glutathione peroxidase (GSHPx) and Na+, K+-ATPase as well as Ca2＋－ATPase were increased (P＜0.05, respectively), while malondialehyde (MDA) was decreased to 42.5% (P＜0.01) during brain ischemia－reperfusion.　Conclusion:The results suggested that THP can protect the rat against ischemia－reperfusion induced brain lesion.