Pulmonary artery hypertension is a disease with complicated pathogenesis, which is characterized by enhanced pulmonary artery constriction and arterial wall remodeling, leading to progressive increase of pulmonary vascular resistance and pulmonary artery pressure, then resulting in right heart failure.Many studies have shown that transforming growth factor-β1(TGF-β1) plays an important role in the development of various diseases, especially in cardiovascular and cerebrovascular diseases.TGF-β1 is involved in multiple cellular responses including cell proliferation, differentiation, migration and apoptosis.TGF-β1 participates in pulmonary artery hypertension mainly via promoting the proliferation of pulmonary artery smooth muscle cells as well as inducing the deposition of extracellular matrix and endothelial-to-mesenchymal transition(EndMT) through many signaling, which is mainly dominated by pulmonary artery smooth muscle cells and pulmonary artery endothelial cells.This review mainly introduces the role of TGF-β1 in pulmonary artery hypertension in order to provide potential drug targets and therapeutic strategies for pulmonary artery hypertension.

RhoA belongs to the small G binding proteins Rho subfamily, playing an important role in the various cellular func-tions, including migration, proliferation, adhesion and apopto-sis. Recent data indicate that RhoA/ROCK pathway causes myo-cardial damage by influencing the myocardial energy metabolism, inflammation, and endoplasmic reticulum stress. On the other hand, the activation of RhoA also has a positive role in MIRI. This article reviews the regulatory effect of RhoA on MIRI and its mechanisms, discusses the prospects of RhoA as a novel thera-peutic target for MIRI, and provides new therapeutic treatments and strategies for MIRI.

Systemic lupus erythematosus ( SLE) is a chronic multisystem relapsing-remitting autoimmune disease, which affects human health seriously.There are numerous animal models that have long been employed in an effort to un-derstand the mechanism and treatment of SLE.Animal models of SLE were reviewed and compared in this paper, to provide references for the researchers to choose appropriate models for studying specific pathogenic mechanism and diagnostic crite-ria, searching for targeted treatment interventions and developing potential therapeutic drugs.

Abstrcat:Pulmonary artery hypertension ( PAH) is a cardiopul-monary disease with extensive obliterative changes in the small to midsized pulmonary arterioles. This review summarizes the al-tered inflammation and immune processes underlying the devel-opment of PAH, and discusses inflammatory factors, immune cells, Rho kinase and gene implicated in PAH. Preclinical stud-ies have provided the basis for abnormal immune response in ani-mal models of the PAH, and this paper, based on inflammatory/immune response mechanisms, proposes PAH potential therapeu-tic targets.

Mangiferin also called Chinonin or mango, is mainly extracted from the Anacardiaceae and Gentianaceae plants. As polyphenol compounds, Mangiferin shows a strong antioxidant activity and a variety of pharmacological effects. In recent years, laboratory study has identified a variety of pharmacological effects associated with Mangiferin including preventing diabetes and its complications, regulating lipid metabolism abnormalities, antitumor, cardiovascular protection,anti hyperuricemia, neuro-protection, anti oxidation, anti-inflammation, antipyresis and analgesia, anti-bacteria and antivirus, antiradiation, liver pro-tection, promoting skeletal growth, anti allergy and immune reg-ulation,etc. In this paper, the research progress of pharmacolog-ical effects of Mangiferin is reviewed, analyzed and summarized in order to provide reference for further research and develop-ment.

Vascular calcification is a process similar to bone de-velopment, which is excessively abnormal deposition of calcium and phosphate in blood vessel wall. It is a sign of early athero-sclerosis formation, and can reduce the atherosclerotic vascular compliance. The common regulation of vascular calcification is affected by many factors. This article discusses the formation of vascular calcification from the molecular mechanism, the chemi- ＜br> cal mechanism and metabolic factors. It also reviews the progress of the prevention of vascular calcification by traditional Chinese medicine.

Myocardial ischemic preconditioning and postconditioning can reduce myocardial infarct size, improve myocardial contractility, protect coronary endothelial and myocardial cell ultrastructure, as well as reduce the incidence of arrhythmias. Clinical practice has confirmed the safety and efficacy of these two methods of myocardial protection. This paper reviewed about ischemic preconditioning and postconditioning protection mechanisms in myocardial ischemia reperfusion injury and clinical research literatures in recent years, to provide a theoretical basis for finding new treatment strategies on the prevention and treatment of ischemic cardiomyopathy.

Salvia miltiorrhiza is dry root or rhizome of the labia-tae plant Salvia miltiorrhiza, whose water-soluble ingredients are recognized as its bioactive components in cardiovascular disea-ses. Based on researches at home and abroad in recent years, this article summarizes pharmacological effect resisting myocardi-al ischemia of Salvia miltiorrhiza ’ s water soluble compounds in multi-level from the prevention, treatment and anti-reperfusion damage, to provide theoretical basis for the research and devel-opment of the active monomers in Salvia miltiorrhiza and com-pound preparations.

Today pedicle screw instrumentation system and short-segment fixation have been commonly used for treatment of thoracolumbar burst fractures because pedicle screw fixation allows 3-column fixation and facilitates simultaneous application of axial compression or distraction and rotational forces.Indirect decompression and direct decompression are the two ways to deal with canal compromise when pedicle screw instrumentation is used.Indirect decompression is achieved to correct the canal compromise due to ligamentotaxis and hyperextension.The present study reviews the current research on indirect spinal canal decompression in adult patients with thoracolumbar burst fracture.

Aim To explore the therapeutical effect and mechanism of baicalein on two 6-hydroxydopamine (6-OHDA ) induced Parkinson′s disease (PD ) rat models,which received unilateral lesions of the left medial forebrain bundle (MFB ) or caudate putamen (CPu ) made by stereotaxic injection of 6-OHDA (MFB-M,CPu-M).Methods PD rat models were established by microinjection of 6-OHDA into MFB or CPu.The anti-tremor effect of baicalein on PD rat models was examined.Spontaneous activity was recor-ded. Dopamine (DA ), dihydroxyphenylacetic acid (DOPAC)and homovanilic acid (HVA)in striatum were quantified by HPLC-ECD.The tyrosine hydroxy-lase (TH)and OX-42 positive cells were detected by immunohistochemical method.The morphological vari-ation of the neurons was confirmed by analysis at an ul-trastructural level.Results Baicalein significantly in-creased the spontaneous activity in CPu-M.The elec-tromyography (EMG ) recordings revealed that com-pared with 6-OHDA group,the tremor frequency in ba-icalein group was decreased by 55% in MFB-M,and by 60% in CPu-M.6-OHDA treatment decreased DA levels in the striatum,while treatment with baicalein attenuated the DA decreases in CPu-M.Moreover,ba-icalein treatment could increase TH-positive neurons and decrease OX-42-postive microglia compared with 6-OHDA group in both MFB-M and CPu-M.Conclu-sions In the present study,it is illustrated that ①microinjection of 6-OHDA into the MFB and the CPu could cause different pathological changes of PD, which is important for efficacy evaluation;②baicalein showed the ability to alleviate the behavior symptoms in PD-rats at different stages by improving motor function and attenuating muscle tremor;③therapeutic effect of baicalein was produced by inhibiting the inflammatory medium production and release,anti-apoptosis,chan-ging dopamine catabolism, and inhibiting dopamine turnover.