Objective To investigate the effects of peptide-binding domain (PBD) of heat shock protein (HSP) 72 on epithelial to mesenchymal transition (EMT) in rat renal tubular epithelial cells.Methods The expressions of wild-type HSP72,mutant of HSP72 lacking peptide binding domain (HSP72-△PBD) and HSP72-PBD were induced by plasmid transfection.NRK-52E ceils were stimulated by TGF-β1 for 48 h.The expressions of α-smooth muscle actin (α-SMA),E-cadherin,HSP72 and Smad3/p-Smad3 were detected by Western blot and immunofluorescence.Results After NRK-52E cells were stimulated by TGF-β 1 (10 μg/L) for 48 h,the expression of α-SMA was increased and the protein level of E-cadherin was decreased.Western blotting and immunofluorescence showed that over-expression of both HSP72 and PBD inhibited TGF-β1-induced up-regulation of protein α-SMA expression,down-regulation of protein E-cadherin.However,overexpression of HSP72-△PBD did not change the protein level of E-cadherin and α-SMA.In addition,over-expression of HSP72 and PBD significantly inhibited the phosphorylation of Smad3.Conclusion Inhibition of Smad3 activation and EMT by HSP72 is associated with the function of PBD.

Xiyanping is used to treat infectious diseases with antibiotics in clinic. The aim of this study is to investigate the mechanism of Xiyanping through studying the effect of the combination of Xiyanping with Cefazolin on the chemotaxis and phagocytic function of peripheral blood neutrophils in mice. Ten healthy mice were in control group. Forty healthy mice in experimental group were infected with staphylococcus aureus, and were randomly divided further into four groups, i. e. model group, Xiyanping group, Cefazolin group and combination group (Xiyanping with Cefazolin). Mice in the control group and model group were given normal saline (NS) through abdomen while those in other groups were given Xiyanping, Cefazolin, and Xiyanping with Cefazolin, respectively. The chemotaxis of peripheral blood neutrophils was detected with the transwell method, and the phagocytic function of peripheral blood neutrophils was analyzed with flow cytometry (FCM). In the present study, there was no significance on the chemotactic index of peripheral blood neutrophils in all the groups (P > 0.05). The actual phagocytotic rate and index of peripheral blood neutrophils in the blank group, Xiyanping group, and the combination group were significantly higher than those of the model group and Cefazolin group (P < 0.05). However, those were not significant in the blank group, Xiyanping group, and the combination group (P > 0.05) or between the model group and Cefazolin group (P> 0.05). Our results suggested the combination of Xiyanping and Cefazolin could enhance the therapeutic effect by improving the phagocytic function of peripheral blood neutrophils.
Animals ; Anti-Bacterial Agents ; pharmacology ; Cefazolin ; pharmacology ; Chemotaxis ; Disease Models, Animal ; Drugs, Chinese Herbal ; pharmacology ; Mice ; Neutrophils ; cytology ; drug effects ; Phagocytosis ; Staphylococcal Infections ; immunology ; Staphylococcus aureus

OBJECTIVE:To optimize the extraction technology for organic acids in Crataegi fructus. METHODS:Based on sin-gle factor test,using liquid-solid ratio,extraction time and ethanol volume fraction as independent variables,extraction yield of or-ganic acids as dependent variable,central composite design-response surface method was used to optimize the extraction technology of organic acids in Crataegi fructus. RESULTS:The optimal extraction technology was as follow as liquid-solid ratio of 18.5:1, adding 75% ethanol,reflux extraction twice,2.0 h each time. Average extraction yield of organic acids in verification test was 5.22%(RSD=2.70%,n=3),with 1.75% relative error of the predicted value(5.13%). CONCLUSIONS:Optimized extraction technology for organic acids in Crataegi fructus is simple,with good reproducibility and predictability.

Objective To analyze the virulence genes and drug resistance in Vibrio parahaemolyti-cus strains isolated in Nantong City from 2015 to 2016 in order to provide reference for the prevention and treatment of Vibrio parahaemolyticus infection and for rational use of medicines. Methods Virulence genes of tlh,tdh and trh in Vibrio parahaemolyticus strains were detected by fluorescence quantitative PCR. Micro-broth dilution method was used to analyze antimicrobial resistance in these strains to 15 kinds of antibiotics. Results Eighty-two Vibrio parahaemolyticus strains were all positive for tlh gene and negative for trh gene and among them,72 carried tdh gene (87.8%). Antimicrobial resistance rates of these strains to ampicil-lin,cefazolin,tetracycline and chloramphenicol were all 1.2% (1/82). Two strains (2.4%) were resist-ant to trimethoprim/sulfamethoxazole. All strains were sensitive or intermediate to another 10 kinds of antibi-otics. Conclusion From 2015 to 2016,Vibrio parahaemolyticus strains carrying virulence genes of tlh and tdh were prevalent in Nantong and no trh gene-positive strains were reported. Except ampicillin, cefazolin, tetracycline,chloramphenicol and trimethoprim/sulfamethoxazole these five kinds of antibiotics, the remai-ning 10 kinds of antibiotics were effective against Vibrio parahaemolyticus and could be used as the treatment of choice.

Hepatocellular carcinoma (HCC) is an aggressive human cancer with increasing incidence worldwide. Multiple efforts have been made to explore pharmaceutical therapies to treat HCC, such as targeted tyrosine kinase inhibitors, immune based therapies and combination of chemotherapy. However, limitations exist in current strategies including chemoresistance for instance. Tumor initiation and progression is driven by reprogramming of metabolism, in particular during HCC development. Recently, metabolic associated fatty liver disease (MAFLD), a reappraisal of new nomenclature for non-alcoholic fatty liver disease (NAFLD), indicates growing appreciation of metabolism in the pathogenesis of liver disease, including HCC, thereby suggesting new strategies by targeting abnormal metabolism for HCC treatment. In this review, we introduce directions by highlighting the metabolic targets in glucose, fatty acid, amino acid and glutamine metabolism, which are suitable for HCC pharmaceutical intervention. We also summarize and discuss current pharmaceutical agents and studies targeting deregulated metabolism during HCC treatment. Furthermore, opportunities and challenges in the discovery and development of HCC therapy targeting metabolism are discussed.