Research progress in pharmacological actions of evodiamine and rutaecarpine is reviewed, including cardiovascular effects, antiplatelet activity, antithrombotic activity, anti invasive and metastatic activity, anti inflammatory activity, antinociception, the effect on the endocrine system and non vascular smooth muscles, anti obese activity and thermoregulatory effect, etc.

Ischemic preconditioning has been defined as a tolerance of the myocardium to subsequent sustained ischemic damage after the heart was insulted one or more brief periods of ischemic stress. The cardioprotective effect of ischemic preconditioning may be mediated by endogenous cardiovascular active substances. Neurotransmitters, including catecholamines, acethylcholine, calci-tonin gene-related peptide and opioids, may be endogenous myocardial protective substances, and participate in the mediation of ischemic preconditioning. Exogenous administration of neurotrans-mitters can mimic the cardioprotective effect of ischemic preconditioning. There is interactions of some neurotransmitters with other endogenous active substances. The mechanism by which neurotransmitters are involved in the cardioprotective effect of ischemic preconditioning is thought to activate their corresponding receptors, with a subsequent triggering cellular signaling pathway, resulting in myocardial protection.

AIM: To observe the protective effects of shenmai injection on myocardial injury induced by 1,1-dipheyl-2-picryl hydrazyl (DPPH)free radic al in isolated rabbit hearts. METHODS: The isolated rabbit hear ts were perfused in a Langendorff model. Left ventricular pressure (LVP), the fi rst derivative of LVP (+dp/dt max ), left v entricular end-diastolic pressur e (LVEDP) and heart rate (HR) were recorded. Coronary flow (CF) and the activity of creatine kinase (CK) in coronary effluent were measured by timed collection of coronary effluent. RESULTS: Perfusion with DPPH ( 0.25 ?mol?L -1 ) for 10 min caused a significant impairment of cardiac functi on, as shown by a decrease in LVP, +dp/dt ma x and HR and an increase in LV EDP as well as the increased release of CK. After perfusion with DPPH ( 0.25 ?mol?L -1 ) for 10 min, treatment with shenmai injection (1320 or 1 160) for 10 min produced a significant improvement of cardiac function and a d ecrease in the release of CK. CONCLUSION: Shenmai injection prot ects against myocardial injury induced by DDPH free radical in isolated rabbit h earts.

OBJECTIVE: The investigation of curing liver disease with stem cell makes a notable performance. This article intends to review the status of clinical and empirical study of stem cell transplants. DATA SOURCES: A computer-based search was conducted in Pubmed for English articles about bone marrow stem cells cure liver ailment published between January 1995 and June 2006 with the Keywords of "bone marrow stem cell, hemopoietic stem cells, mesenchymal stem cells, hepatic fibrosis". Meanwhile, relevant Chinese articles were searched in Chinese Journal Full-text Database with the key words of "bone marrow stem cell, hemopoietic stem cells, mesenchymal stem cells, hepatic fibrosis". STUDY SELECTION: Data were checked in the first trial and articles about the bone marrow stem cell and liver disease therapy are selected, while obvious unrelated literatures or repetitive study were excluded. DATA EXTRACTION: A total of 58 related English articles and 40 Chinese articles were collected, including 36 studies about bone marrow stem cells, 24 researches on mesenchymal stem cells and 14 about hemopoietic stem cells, 30 literatures of them in accordance with the inclusion criteria were reviewed. DATA SYNTHESIS: There are all kinds of stem cells in bone marrow that can differentiate other kinds of cells, including mesenchymal stem cells and hemopoietic stem cells. Both animal trials and clinical researches show that hemopoietic stem cells can differentiate into liver cells and hepatic oval cells and is mature to participate in the liver regeneration. Mesenchymal stem cells are homogeneous cells with multi-differentiation potentials and can be differentiated into liver cells and bile duct cells. Bone marrow stem cell therapy has many merits than traditional methods, for example simple materials, culture in vitro, passage and easy amplification, indicating a great achievement in clinic. CONCLUSION: We can use bone marrow stem cell therapy for all kinds of refractory hepatopathy, such as hepatitis, liver cirrhosis and hepatoma etc. It will not only improve haematogenesis and immune function, but also replace necrosis and lost hepatic cell, leading a perfect boundary of hepatopathy therapy.

BACKGROUND:A cell mass from bone marrow can transform into oval cells and then differentiate into hepatocytes and biliary tract endothelial cells.It will bring a new hope for repairing irreversible damage of the liver.OBJECTIVE:To review several recent research results of the differentiation of bone marrow stem cells into hepatocytes.RETRIEVAL STRATEGY:A computer-based search was conducted in Pubmed and HighWire for English articles about bone marrow stem cells for liver ailments published between January 1999 and June 2007 with the key words of "bone marrow stem cells,mesenchymal stem cells,hemopoietic stem cells,hepatocytes,hepatic fibrosis,hepatic cirrhosis".Meanwhile,Vip Database was undertaken to identify the relevant articles on bone marrow stem cells in the treatment of hepatic cirrhosis and hepatic fibrosis published between January 1999 and June 2007 with the key words of "bone marrow stem cells,mesenchymal stem cells,hemopoietic stem cells,hepatocytes,hepatic fibrosis,hepatic cirrhosis" in Chinese.The data were selected primarily,and then quotations of each article were checked.Inclusive criterion:The articles related to curing hepatic fibrosis and hepatic cirrhosis with bone marrow stem cells were selected.Exclusive criteria:the articles with repetitive research or Meta analysis were excluded.A total of 49 related English articles and 42 Chinese articles were collected,34 literatures of them in accordance with the inclusive criterion were reviewed.Fifty-seven articles with old or repetitive articles were excluded.LITERATURE EVALUATION:Of the 34 inclusive articles,18 were on transplanting in vivo,12 were about cultivation and induction in vitro and 4 were about the problems and prospect.DATA SYNTHESIS:Bone marrow stem cells include mesenchymal stem cells and hemopeietic stem cells,which are characterized by plasticity.Growth factors in vitro and special microenvironment in vivo could induce the differentiation of bone marrow stem cells into the precursor of hepatocytes and mature hepatocytes.Moreover,hepatic function could be improved obviously.The superiorities of bone marrow stem cells included affluent source,low cost,little injury,without embolism and graft rejection in autologous transplantation,which offer a new style for curing hepatic diseases.Bone marrow stem cells would be the cell resource of artificial liver.CONCLUSION:Using bone marrow stem cells therapy for all kinds of refractory hepatopathy,such as hepatitis,liver cirrhosis and hepatoma,indicates a great achievement in clinic.

In recent years,the prevalence of diabetes has increased rapidly,and which has become a serious public health problem worldwide.Diabetic nephropathy is a major cause of end-stage renal failure,which is also one of the most common chronic complication of diabetes.However,the pathogenesis of diabetes and diabetic nephropathy has not been fully elucidated up to now.IL-17 plays a key role in autoimmune disease and inflammatory disease.This article reviews the role of IL-17 in the pathogenesis of diabetes and diabetic nephropathy.

BACKGROUND:Bone marrow mesenchymal stem cel s can be differentiated into myocardial cel s induced by 5-azacytidine in vitro, which provides an opportunity for cel transplantation in the treatment of heart disease. OBJECTIVE:To study the induction effects of 5-azacytidine at different concentrations on the myocardial differentiation of bone marrow mesenchymal stem cel s in rats. METHODS:Passage 3 bone marrow mesechymal stem cel s were incubated with DMEM containing 0, 5, 10, 20μmol/L 5-azacytidine for 24 hours, and then the induced medium was replaced by DMEM containing 5%fetal bovine serum for subsequent 28-day culture. Afterwards, expression of cardiac troponin I was detected by immunocytochemical method. RESULTS AND CONCLUSION:Cel death occurred at 24 hours after 5-azacytidine induction, which was more obvious in the 20μmol/L group than the 5 and 10μmol/L groups. The positive expression of cardiac troponin I was significantly lower in the 5μmol/L group than the 10 and 20μmol/L groups (P<0.05), but there was no significant difference between the 10 and 20μmol/L groups (P>0.05). These experimental findings indicate that 5-azacytidine can induce the differentiation of rat bone marrow mesenchymal stem cel s into myocardial cel s in vitro, and its optimal concentration is 10μmol/L.

BACKGROUND: Hepatic fibrosis is a reversible disease, interfering in course of disease promptly can decrease hepatic cirrhosis and fatal complication. Hepatic stellate cells (HSCs) is a key factor in pathogenesy of hepatic fibrosis.OBJECTIVE: To investigate the effects of Shugan granule on HSCs activation and trans-membrane signal transduction stimulated by transforming growth factor beta 1 (TGF-β1) in rats, and to explore the anti-fibrosis mechanism.DESIGN, TIME AND SETTING: Controlled observational trials based on cytology were performed in the Central Laboratory of Molecules, Luzhou Medical College between June 2008 and February 2009. MATERIALS: HSC-T6 cell line was purchased from Institute of Liver Diseases, Shanghai University of Traditional Chinese Medicine, its phenotype was the activated hepatic stellate cells. Shugan granule was offered by Drug Institute, Affiliated Hospital of Luzhou Medical College at a Batch No. 20071120.METHODS: The influence of different concentrations (0.01, 0.02, 0.04, 0.08 g/L) of Shugan granule on HSCs proliferation was determined by MTT. 0.01 g/L was defined as the dose of Shugan granule contributing no influence on cell proliferation. HSCs were cultured in a culture plate and then divided into 4 groups: control group without management, TGF-β1 group with 5 μg/L TGF-β1 solution in culture medium, Shugan granule group with 0.01 g/L Shugan granule in a culture medium, and TGF-β1 + Shugan granule group with 5 μg/L TGF-β1 solution and 0.01 g/L Shugan granule in culture medium. MAIN OUTCOME MEASURES: Morphological features of HSCs were detected by microscopic. Immunohistochemical method was used to detect the expression of Smad3 and Smad7 in HSCs. RT-PCR was applied to observe the HSCs activation and trans-membrane signal transduction. RESULTS: ①The cell morphology of TGF-β1 group was similar with that in the control group, and the extension was more obvious. In the TGF-β1 + Shugan granule group, the cell morphology was close to that in TGF-β1 group. There was no karyopyknosis or apoptosis observed in each group. ②Immunohistochemical method showed the expression of Smad3 and Smad7 in control groups were increased. TGF-β1 could slightly increase the expression of Smad3 and Smad7 (P < 0.05), while Shugan granule group and TGF-β1 + Shugan granule group increased the expression of Smad7 significantly, accounting for 1.99 times compared with control group (P < 0.01). ③RT-PCR result showed that Shugan granule could increase the expression of Smad7 (P < 0.05), but the expression of Smad3 was not regulated. 5 μg/L TGF-β1 could up-regulate the expression of Smad3 and Smad7 (P < 0.05). In the TGF-β1 + Shugan granule group, Smad7 expression was increased by 101% (P < 0.05), but Smad3 transcriptional level was not changed(P > 0.05). CONCLUSION: ①TGF-β can stimulate the gene expression of Smad3 and Smad7, it also obtain a balance of feedback regulation mechanism between R-Smads and I-Smads. ②Shugan granule may prevent and cure hepatic fibrosis through decreasing the proliferation of HSCs in a dose-dependent manner. ③Shugan granule can inhibit the TGF-β-Smad signaling pathway through increasing the expression of Smad7.

AIM:To determine whether apoptosis is involved in the development of vascular remodeling in renovascular hypertension rats and whether the inhibitory effect of tetrandrine on proliferation is mediated by apoptosis.METHODS:Apoptosis was detected in histologic sections of aorta and tail arteries with in situ end-labeling.The apoptosis ratio in cultured cells was measured by [3H]-TdR incorporation and flow cytometer analysis method.RESULTS:Compared with the sham group,the apoptosis rate of renal hypertension rat(RHR)increased.Tetrandrine(Tet)directly induced apoptosis in cultured AVSMCs(from RHR)and increased apoptosis induced by TGF?,TGF?1 and deficient FCS.CONCLUSION:Tet induces and sensitizes vascular smooth muscle cells of RHR to apoptosis,which at least partly related to the regression of vascular remodeling.

Objective To investigate whether the protection of ischemic preconditioning (IPC) against myocardial ischemia/reperfusion (I/R) injury is mediated by toll-like receptor 4(TLR4)/NF-kB pathway,and whether these effects are related to the release of calcitonin gene-related peptide (CGRP).Methods Sprague-Dawley rats were subjected to 60 min of ligation of the left anterior descending coronary artery followed by 3 h of reperfusion to induce I/R injury.IPC was performed by 4 cycles of 3-min left coronary artery occlusion followed by 5-min reperfusion before the I/R.The expression of TLR4 mRNA was determined by RT-PCR.TLR4 and NF-kB protein expression were analyzed by immunohistochemistry.Myocardial infarct size,CGRP concentration in plasma and activity of creatine kinase in serum were also measured.Results IPC significantly reduced the infarct size and creatine kinase activity concomitantly with the increase in plasma CGRP concentration.The expressions of TLR4 protein and mRNA and NF-kB protein were increased by myocardial I/R injury,and dramatically inhibited by IPC.Conclusion IPC protects against myocardial I/R injury by inhibition of TLR4/NF-kB pathway.These effects are related to the increased the release of CGRP.