Neuronal guidance factor Netrin-1 has been known to be involved in nervous system development by controlling neuronal migration through both chemoattractive and chemo-repulsive signaling by binding different receptors. Netrin-1 has been shown to play a positively regulatory role during inflammatory process recently. Since the chemorepulsive receptors were found in leukocytes, it is suggest that Netrin-1 played a protective role in tissue through inhibiting leukocyte trafficking and accumulating during inflammatory process in researches. It is demonstrated that Netrin-1 can limit inflammatory response through the involvement of inflammatory cascades, attenuate hypoxia-inducible tissue injury and suppress apoptosis concurrently. It is indicated that Netrin-1 can be a novel target in future through preventing and inhibiting inflammatory diseases in these researches. This review will focus on recent relevant advances and in-depth study to elucidate its mechanism of anti-inflammation.

Objective To explore the early diagnosis of lower extremity deep venous thrombosis (LDVT)and evaluate the therapeutic effect of anticoagulant therapy in hospitalized patients with acute ischemic stroke. Methods　According to Wells model for suspecting lower extremity deep venous thrombosis,patients with suspected LDVT were confirmed by compression ultrasonography. If the patients diagnosed with LDVT had no contraindications to anticoagulant therapy,they were treated with low molecular weight heparin(LMWH)subcutaneous injection and oral warfarin at the same time.The dosage of oral warfarin was determined by Roberts'age adjusted warfarin loading protocol.LMWH was stopped when the patients'international normalized ratio(INR)was 2.0～3.0 for two consecutive days. Results From January 2003 to August 2007,2067 cases with acute ischemic stroke were admitted to the department of neurology in Huizhou Municipal Central Hospital including 18 cases with LDVT and the incidence was 0.9%.The patients with LDVT all had paralytic extremities including 13 left legs and 5 right legs with deep vein thrombosis.All the 18 cases were treated by anticoagulant including 17 cases with oral warfarin treatment for 3 months.Symptoms in all LDVT patients were eliminated.12 cases had been observed for one year and 5 cases for three months after they stopped taking warfatin.There were no patients with pulmonary thromboembolism and LDVT recurrence. Conclusions　By using Wells model for suspecting LDVT,patients with acute ischemic stroke-complicated LDVT can be timely diagnosed.The goal of prompt and enough anticoagulant can be achieved according to Roberts'age adjusted warfarin loading protocol.Because of racial difference,population difference and other unknown factors,the incidence of acute ischemic stroke patients with complicated LDVT is much lower in Huizhou.It suggests that it should be unnecessary to use LMWH in patients with acute ischemic stroke to prevent LDVT in Huizhou.

Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is a common respiratory disease in clinic, and with a pathological manifestation of pulmonary edema, decreased pulmonary compliance as well as pulmonary epithelial/endothelial cells injury. At present, it was suggested that systemic inflammatory response syndrome (SIRS) caused by various causes which play an important role in the occurrence and development of ALI/ARDS. Widely activated neutrophils can migrate to lung tissue and release plenty of proteases in the procedure of SIRS, including neutrophil serine proteases (NSPs), lysozyme, myeloperoxidase and collagenase, which can induce severe lung injury. Meanwhile, NSPs, such as neutrophil elastase (NE), cathepsin G (CG), proteinase 3 (PR3) and neutrophil serine proteinase 4 (NSP4), are important in the pathogenesis of ALI/ARDS. Therefore, Serpins may protect lung tissue by inhibiting NSPs. However, the specific mechanism of Serpins is not totally clear. In this article, we will discuss the mechanism of action of NSPs in the inflammatory response of ALI/ARDS, the structural overview of Serpins, the primary role of Serpins in ALI/ARDS,such as the inhibition of NSPs activity, other roles of Serpins in ALI/ARDS, such as the inhibition of inflammatory factor release, regulation of apoptosis and protection of vascular endothelial cells and pulmonary surfactant-associated glycoprotein D (SP-D), and the clinical application of exogenous Serpins in ALI/ARDS to explore the role of Serpins in the pathogenesis of ALI/ARDS. The aim is to provide new ideas and strategies for the clinical treatment of ALI/ARDS.

Objective To investigate the effect of complement C3a on mouse podocytes phenotype transformation.Methods Purified C3a recombinant protein was used to stimulate mature mouse podocytes.The expression of the mature podocyte markers synaptopodin,podocin,nephrin,CD2-associated protein (CD2AP) and the mesenchymal cell markers fibroblast specific protein 1 (FSP-1),α-smooth muscle actin (α-SMA) were detected by RT-PCR,Western blotting,immunochemistry and immunofluorescence,respectively.Some podocytes were transfected with integrin-linked kinase (ILK) siRNA before the administration of C3a,the expression of nephrin and α-SMA were accessed by Western blotting,and the expression of Snail and α-actinin 4 were accessed by Western blotting and immunochemical method.The migration ability of podocytes was observed by scratch test.Results Immunocytochemistry and immunofluorescence analysis showed that synaptopodin,podocin,nephrin,CD2AP were highly expressed by mature mouse podocytes.The expression of these podocyte markers could be markedly inhibited after 24 h of C3a (0.1 μmol/L) treatment,and accompanied by the induction of mesenchymal markers FSP-1 and α-SMA.Compared with control group,the mRNA levels of synaptopodin,podocin,CD2AP and nephrin were significantly repressed by the administration of C3a in a dose-dependent manner,whereas the transcription of FSP-1 and α-SMA were remarkably up-regulated by C3a treatment (P ＜ 0.05,respectively).Western blotting analysis also confirmed the decrease of synaptopodin,podocin,nephrin and CD2AP protein and the increase of FSP-1 and α-SMA protein were closely depend on the C3a concentration (P ＜ 0.05,respectively).To further assess the downstream of C3a,some podocytes were transfected with ILK siRNA before the administration of C3a.Compared with C3a group,the protein levels of nephrin and α-SMA were significantly changed by the administration of ILK siRNA (P ＜ 0.05,respectively).The expression of α-actinin 4 and Snail induced by C3a were inhibited by ILK knockdown (P ＜ 0.05,respectively),accompanied by a decline of cell migration potency.Conclusion Complement fragment C3a can induce transformation of mouse podocytes to mesenehymal cells,and ILK signaling pathway is involved in this cell type transformation.