Chemokine is a small protein which plays an impor-tant role in men's physiological function.It has chemotactic ac-tivity and is often secreted by immune cells and glial cells like microglia or astrocytes.Through the effect of chemokine recep-tors on target cells,various immune cells can achieve directional migration and play an important role in the diseases related with immunity and inflammation.CCL2,also known as monocyte chemotactic protein-1 (MCP-1 ),is one member of chemokine CC subfamily (βsubfamily).It can chemokine monocytes, macrophages and T lymphocytes to affect their phagocytosis func-tion and produce antibodies to combat invading microorganisms. In recent years,it has been found that CCL2 plays a key role in the occurrence and development of the problems concerning cen-tral nervous system and immune system as well as cancer, AIDS,leukemia,diabetes and other diseases.This thesis is to give an elaboration on the latest research on CCL2 and the rele-vant diseases.

Discovery of noncoding RNA(ncRNA)over the past decade has reflected a paradigm shift of traditional RNA research. There is evidence that RNA can function not only as a messenger between DNA and protein,but as a regulator of genome organization and gene expression,which is increasingly elaborate in complex organisms. ncRNA seems to operate at many levels,however,in?cluding the physiological and pathological status. The research of ncRNA in pharmacology has not been summarized before. Here,we reviewed the emergence of the ncRNA in the research of pharma? cology,such as acting as biomarkers and medical targets. Besides,we mentioned their role in drug resistance and drug addiction in order to highlight the significant role of ncRNA in pharmacology.

Asthma is a chronic inflammatory respiratory disease accompanied with airway inflammation, airway remodeling and bronchial hyperresponsiveness. Chemokines are important for the recruitment of immune cells to the lung, which play an important role in the formation and development of asthma. Targeting the chemokine receptors to anti-inflammation and anti-asthma is a new strategy and some candidate drugs are discovered recently. This review is focused on the development of chemokine receptor antagonists for anti-asthma, which will promote the compound designations.

Pyk2(Proline-rich tyrosine kinase 2) is an important member of focal adhesion kinase family. Pyk2 is highly ex-pressed in the central nervous system and the hematopoietic sys-tem . Pyk 2 can trigger a variety of SH 2 domain-containing pro-
teins to phosphorylate their substrates, thus it can participate in the regulations including ion channel activation, stress response, cell adhesion, cytoskeleton reorganization, vesicle transport and so on. Through the regulations above, the ability of cell migra-tion, survival, proliferation changes accordingly, suggesting that Pyk2 in many important regulatory processes may become a tar-get for clinical effects. Current drug development for Pyk2 main-
ly focuses on cancer, osteoporosis and immune response. This review illustrates the domain structure, regulatory mechanisms, potential drug targets, and the drug development of Pyk2 based on the above three fields, which will provide a theoretical basis for clinical treatment.

The latest literatures showed that the anti-platelet aggregation drugs had a good application in cardiovascular disease, however still with hemorrhage side effects and some new drugs' mechanism was unknown. So further investigations on the mechanism of anti-platelet aggregation are necessary to discover a new type of anti-platelet drugs, such as antagonists of the EP3 receptor.

ObjectiveTo study the effects of Morroniside on platelet aggregation in rabbits induced by Adenosine diphosphate (ADP), Arachidonic acid (AA), Platelet activating factor (PAF). MethodsThe platelet aggregation was determined by Born's method. ResultsCompared with the controls, Morroniside inhibited platelet aggregation induced by ADP, AA, PAF （P<0.001）and especially selective on ADP. ConclusionMorroniside inhibited platelet aggregation in rabbits, especially induced by ADP.

Abstract:Aim To study the effect of rotenone on α-synuclein in rat midbrain of Parkinson's disease(PD).Methods Rats were subcutaneouly injected with chronic low dose rotenone(1.0 mg·kg~(-1)·d~(-1)).Movements within 5 minutes were evaluated in open field test.Tyrosine hydroxylase(TH)-positive neuronsin the midbrain were measured with immunofluorescence staining.α-SYN protein level in the midbrain was demonstrated with immunohistochemical staining and Western blot.Results Compared to the control group,latency time,crossing,rearing and rearing time were changed significantly(P<0.05,0.01)in the rotenone group,TH-positive neurons were reduced(P<0.05)and α-SYN protein level in the midbrain was increased(P<0.05).Conclusion Injection with rotenone can induce PD symptom,which may be correlated to α-SYN protein level in the midbrain.

This study is to investigate the amelioration effect of glucocorticoid receptor (GR) antagonist mifepristone on the changes of learning and memory abilities in rat model of depression. In the present study, a 35-day rat chronic unpredictable stress (CUS) model was used to observe both depression-like behaviors with sucrose preference test and open-field test and learning and memory-associated behaviors with Morris water maze test. A total of 45 male adult Sprague-Dawley rats were randomly assigned to three groups of equal size: control group (CON); CUS group (CUS); CUS + mifepristone group (CM). Animals in CM group were first exposed to CUS for 14 days, and then were administered with 50 mg x kg(-1) x d(-1) of mifepristone with continued CUS procedure. Corticosterone EIA Kit was used to detect the concentration of plasma corticosterone (CORT). Nissl staining was used to observe the structure of hippocampus. The results demonstrated that CUS exposure induced both depressive-like and learning and memory-associated behaviors and these deficits were reversed by mifepristone. Compared to CON group, the concentration of plasma CORT increased significantly in CUS group. CUS exposure damaged the structure of hippocampus, whereas mifepristone had an amelioration effect. Together, the structural deficits of hippocampus resulting from long-term stress exposure, which could contribute to the impairment of learning and memory in depression, are reversed by the GR receptor antagonist mifepristone.

Aim To investigate the role of chemokine-like factor 1 ( CKLF1 ) in SH-SY5 Y cell migration and its molecular regulatory mechanism. Methods SH-SY5Y cells were stimulated with CKLF1 for 0. 5 h, 2 h, 8 h and 24 h, respectively. The migration distance and the percentage of migration cells were recorded by CELLocate analysis. The phosphorylation of focal ad-hesion kinase ( FAK) at Tyr-397 site was detected by Western blot analysis. By chemotaxis assays, we con-firmed the chemotaxis of CKLF1. Furthermore, FAK inhibitor PF-573228 and PLCγ inhibitor U73122 were used for the research of molecular regulatory mecha-nisms involved. Results CKLF1 promoted cell migra-tion and induced a strong increase in the phosphoryla-tion level of FAK-pY397 , which were significantly at-tenuated by the presence of U73122 ( a specific inhibi-tor for PLCγ) . In addition, the chemotaxis of CKLF1 was obviously blocked by the FAK inhibitor PF-573228 . Conclusion CKLF1 induces SH-SY5 Y cell migration via PLCγ/FAK signaling pathway.

Aim To study the effect of synapsinⅠon synaptic transmission in rat dentate gyrus induced by(-) clausenamide.Methods The basal synaptic transmission experiment was conducted through electrophysiological recordings.The effect of(-) clausenamide on synapsinⅠ phosphorylation was measured by western blot and confocal microscopy.Results(-)Clausenamide increased the population spike(PS) of hippocampal dentate gyrus.The phosphorylation of synapsinⅠ was increased both in cortex and hippocampus,the maximum effect was observed at 5 min in hippocampus and at 15 min in cortex.Furthermore,(-)clausenamide promoted the phosphorylation of synapsinⅠat a dose-denpendent manner in PC12 cells.The phosphorylation of synapsinⅠ in PC12 cells and synaptosomes incubated with(-)clausenamide was increased and reached maximum at 1~2 min.However,H89,PKA inhibitor,blocked the effect of(-)clausenamide on synapsinⅠ phosphorylation.Conclusion(-)Clausenamide activated synapsinⅠ via PKA signal pathway,which may contribute to the effect of(-)clausenamide on potentiating basal synaptic transmission.