The function of the nervous system is largely determined by the communication between neurons and glial cells.The interaction of complex signaling pathways between neurons and glial cells involves in a variety of signaling molecules.Purines and the purinergic receptors play a crucial role in the process of the interaction.For a long time, the study on the central nervous system is mainly focused on neurons, while glial cells are mainly used as support cells or in response to brain injury to provide a guiding role.The latest research shows that glial cells play an important role in the occurrence and development of nervous system diseases.We will summarize the function of purinergic receptors in the interaction of neurons and glial cells and in neurological diseases.

Long noncoding RNAs ( lncRNAs ) are transcribed RNA molecules greater than 200 nucleotides in length. In recent years, studies have shown that lncRNAs have many important bi-ological functions. With the development of modern biological technology, lncRNAs transcripts can be easily detected and pre-dicted. However, unlike protein-coding genes whose sequence motifs usually have indicative function, lncRNA sequence infor-mation is currently uninformative for function prediction. Thus, how to decode the function of lncRNAs has gradually become a hot issue in genome research. The paper summarizes the studies regarding the methods to probe the function of lncRNAs.

Objective To investigate the relationship between mRNA expression of DMBT1 in breast cancer tissues and clinicopathological characteristics of patients with breast cancer.Methods 60 cases of breast cancer tissues,30 cases of breast paracancerous hyperplasia tissues and 30 cases of breast paracancerous normal tissues were selected,then reverse transcription-polymerase chain reaction (RT-PCR) were performed to detect the differential expression of DMBT1 in mRNA levels.Furthermore,its relationship with clinicopathological characteristics of patients with breast cancer was analyzed.Results 44 out of 60 breast cancer tissues were detected no or low expression of DMBT1 (73.3％),and 16 out of 60 cases were found normal expression of DMBT1(26.7％).There were statistically significant differences between paracancerous normal tissues and breast cancer tissues,also between paracancerous hyperplasia tissues and breast cancer tissues (x2 =11.72,P =0.000 62 ; x2 =15.99,P =0.000 06).No significant difference was found between the low expression of DMBT1 with the age of patients (x2 =1.733,P =0.188),the size of tumor (x2 =0.776,P =0.378) and the histological grade of tissues (x2 =1.000,P =0.316).However,the loss rates of DMBT1 mRNA expression in patients with lymph node metastasis and clinical stage Ⅲ were higher than that in patients without metastasis and clinicalⅠ-Ⅱstage (x2 =4.885,P =0.026 ; x2 =4.600,P =0.032).Conclusion Low expression of DMBT1 mRNA is closely associated with the metastasis and clinical stage of breast cancer.

Endothelial progenitor cells (EPCs) can differentiate into mature endothelial cells and participate in postnatal vascular regeneration and impaired endothelium repair.Rearches in recent years on use of EPCs as seed cells in promoting angiogenesis,maintaining the integrity of endothelial function and constructing tissue engineered blood vessels are reviewed.

Investigations and interviews on six county (city)-level public hospitals practicing the drug zero price margin policy discovered increases on average outpatient expense per visit,average outpatient drug expense per visit,ratio of outpatient drug expense,average drug expense per hospital discharge,and ratio of drug expense upon discharge as well as the total ratio of drug expenses.An analysis of the poor performance of the policy results in the following recommendations.A better performance of this policy calls for support of such reforms as drug supply manner,drug price control,doctors' incentives for over-prescription and payment manner at public hospitals.Only with these support can this policy reach its expected outcomes of alleviating the drug expense burden of the people.

Purinergic receptors are divided into P1(adenosine)and P2(ATP)receptors.P2 receptor are divided into two subtypes,namely P2X(ligand-gated ion channels)and P2Y(G-protein coupled)receptors.Several kinds of purinoceptor subtypes have been expressed in endocrine pancreas and participate in regulating the secretion of insulin.Purinoceptor and ligand are correlated with pathogenesis of diabetes mellitus and complications and make it possible to provide a new target to treat diabetes mellitus and complications.

Objective:To explore the hepatoprotective effect and its mechanism of the geraniin on mice with acute liver injury induced by D-galactosamine (D-GalN). Method:A total of 60 Kunming mice were randomly divided into normal group, model group, Silymarin group (positive group 180 mg·kg^-1), and low, medium and high-dose geraniin groups (50, 100, 200 mg·kg^-1). All the mice were given with saline or corresponding dose of drugs (10 mL·kg^-1) by gavage once a day for 10 d. After 2 h of the last administration, except the normal group, the mice of other groups were injected intraperitoneally with D-GalN (500 mg·kg^-1) to induce the acute liver injury. After 16 h, the eye balls of mice were removed to take blood, and all mice were put to death to collect samples of liver. Activity or content of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total bilirubin (TBIL), malondialdehyde (MDA), total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-Px) in liver were determined by biochemical method. The serum levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), γ-interferon (IFN-γ) and interleukin-6 (IL-6) were detected by enzyme-linked immunosorbent assay (ELISA), and expressions of Toll-like receptor-4(TLR-4) and nuclear factor(NF)-κB proteins were detected by Western blot. Liver histopathological changes were observed by hematoxylin-eosin (HE) staining. Result:Compared with the normal group, the serum levels of ALT, AST, ALP, TBIL and liver MDA in the model group were significantly increased (P<0.05, P<0.01). Compared with the model group, geraniin can reduce activities or contents of ALT, AST, ALP, TBIL in serum and MDA in liver of mice (P<0.05, P<0.01), but increase activities of T-SOD and GSH-Px in liver (P<0.05,P<0.01), while inhibiting the contents of TNF-α, IL-1β, IL-6, IFN-γ and the expressions of TLR-4 and NF-κB proteins in serum (P<0.05,P<0.01). HE staining showed that acute liver injury of mice was alleviated obviously by geraniin. Conclusion:Geraniin has an obvious protective effective on acute liver injuries induced by D-GalN in mice. Its mechanism may be correlated with oxidative stress, inflammation and TLR-4/NF-κB signaling pathway.

Objective:To explore the mechanism of gentiopicroside （GPS） in preventing acute liver injury induced by carbon tetrachloride （CCl₄） in mice and its effect on the Toll-like receptor 4 （TLR4）/myeloid differentiation factor 88 （MyD88）/nuclear factor-κB （NF-κB） signaling pathway. Method:Sixty mice were randomly divided into a normal control group， a model group， a silymarin group （150 mg·kg^-1）， and high- （200 mg·kg^-1）， medium- （100 mg·kg^-1）， and low-dose （50 mg·kg^-1） GPS groups， with 10 in each group. The mice in the groups with drug intervention were administered correspondingly by gavage at 10 mL·kg^-1， and those in the normal control group and the model group receive an equal volume of distilled water， once per day. Ten days after administration， mice in the normal control group were subjected to the intraperitoneal injection of peanut oil （10 mL·kg^-1） and those in other groups were injected with peanut oil （10 mL·kg^-1） containing 0.12% CCl₄ for the induction of acute liver injury model. After fasting for 16 hours， blood was collected from eyeballs and liver tissues were collected. Hematoxylin-eosin （HE） staining was used to observe the pathological changes of liver tissues. The content or activities of alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， total bilirubin （TBIL）， alkaline phosphatase （ALP）， total superoxide dismutase （T-SOD）， and γ-glutamyl transpeptidase （γ-GT） in the serum， malondialdehyde （MDA） and glutathione peroxidase （GSH-Px） in liver tissues were determined by biochemistry techniques. The levels of tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， and interleukin-6 （IL-6） in liver tissues were measured by enzyme-linked immunosorbent assay （ELISA）. Western blot was used to detect the protein expression of TLR4， MyD88， and NF-κB in liver tissues. The expression of phosphorylated NF-κB （p-NF-κB） was detected by immunohistochemistry. Result:Compared with the normal control group， the model group showed increased levels of ALT， AST， ALP， TBIL， γ-GT， and MDA （P<0.01）， and blunted activities of T-SOD and GSH-Px （P<0.01）. Compared with the model group， the high- and medium-dose GPS groups exhibited declining levels of ALT， AST， ALP， TBIL， γ-GT， and MDA （P<0.05， P<0.01） and potentiated T-SOD and GSH-Px activities （P<0.05， P<0.01）. Compared with the normal control group， the model group displayed elevated levels of TNF-α， IL-1β， and IL-6 in liver tissues （P<0.01） and increased protein expression of TLR4， MyD88， and p-NF-κB （P<0.01）. Compared with the model group， the high- and medium-dose GPS groups showed decreased TNF-α， IL-1β， and IL-6 content in liver tissues （P<0.05， P<0.01） and dwindled TLR4， MyD88， and p-NF-κB protein expression （P<0.05， P<0.01）. Conclusion:GPS possesses a protective effect on mice with acute liver injury induced by CCl₄， and its mechanism of action may be related to the regulation of TLR4/MyD88/NF-κB signaling pathway and inhibition of oxidative stress.

Alcoholic liver disease(ALD), with its increasing morbidity and mortality, has seriously and extensively affected the health of people worldwide. Methyl ferulic acid(MFA) has been proven to significantly inhibit alcohol-induced lipid production in L02 cells through the AMP-activated protein kinase(AMPK) pathway, but its in-depth mechanism remains unclear. This study aimed to further clarify the mechanism of MFA in improving lipid accumulation in L02 cells through the microRNA-378b(miR-378b)-mediated calcium/calmodulin-dependent protein kinase kinase 2(CaMKK2)-AMPK signaling pathway based on existing researches. L02 cells were induced by 100 mmol·L~(-1) ethanol for 48 h to establish the model of ALD in vitro, and 100, 50, and 25 μmol·L~(-1) concentration of MFA was treated. MiR-378b plasmids(containing the overexpression plasmid-miR-378b mimics, silence plasmid-miR-378b inhibitor, and their respective negative control-miR-378b NCs) were transfected into L02 cells by electroporation to up-regulate or down-regulate the levels of miR-378b in L02 cells. The levels of total cholesterol(TC) and triglyceride(TG) in cells were detected by commercial diagnostic kits and automatic biochemical analyzers. The expression levels of miR-378b in L02 cells were detected by real-time quantitative polymerase chain reaction(qRT-PCR). CaMKK2 mRNA levels were detected by PCR, and protein expressions of related factors involved in lipid synthesis, decomposition, and transport in lipid metabolism were detected by Western blot. The results displayed that ethanol significantly increased TG and TC levels in L02 cells, while MFA decreased TG and TC levels. Ethanol up-regulated the miR-378b level, while MFA effectively inhibited the miR-378b level. The overexpression of miR-378b led to lipid accumulation in ethanol-induced L02 cells, while the silence of miR-378b improved the lipid deposition induced by ethanol. MFA activated the CaMKK2-AMPK signaling pathway by lowering miR-378b, thus improving lipid synthesis, decomposition, and transport, which improved lipid deposition in L02 cells. This study shows that MFA improves lipid deposition in L02 cells by regulating the CaMKK2-AMPK pathway through miR-378b.
Humans ; Ethanol/toxicity* ; AMP-Activated Protein Kinases/metabolism* ; Fatty Liver ; Triglycerides ; MicroRNAs/genetics* ; Calcium-Calmodulin-Dependent Protein Kinase Kinase/genetics*

Aim To investigate whether DCP has pro- teetive effeet on 2 ,4-dimethylnitrosamine ( DMN) -induced liver fibrosis rat model and its effect on MAPK signaling pathway.Methods Hats were intraperitoneal ly injected with DMN to establish HF model,and then were randomly divided into five groups, namely model group, colchicine group, DCP low-dose, medium-dose and high-dose groups,and control group.The rats were given DMN continuously for six weeks.Serum was col-lected afterwards to detect biochemical indexes of liver function.HE and Masson staining and immunohisto- chemical experiments were performed on liver tissues.RT-PCR was applied to detect the expression of inflammatory factors.Western blot was used to detect the ex pression of proteins related to MAPK pathway,the preventive effect of DCP on HF was observed, and its in-tervention effect on MAPK pathway was explored.Results The liver function of rats in model group was severely impaired, with obvious hepatocyte damage, inflammatory cell infiltration and increased interstitial fibrosis , suggesting that the preparation of HF model was successful.Conclusions DCP can interfere with MAPK signaling pathway to inhibit the inflammatory response and alleviate the progression of HF in rats.