Chelating ligand method has been used to synthesize baicalin-metal (Ni2+, Co2+, Cu2+) complexes (BMC). The composition and structure of BMC were characterized by the element analysis, ultraviolet spectrum (UV), infrared spectrum (IR), mass (MS) and thermal gravitational analysis (TGA). MTT was used to analyze the effects of BMC on SMMC-7721 cell proliferation. PI staining method and Annexin-V/FITC double staining method were used to analyze the effects of BMC on the cell cycle and apoptosis of SMMC-7721 cell. Fluorescence quantitative RT-PCR was used to analyze the expression of BMC on Bcl-2 gene and Bax mRNA, flow cytometry was used to analyze BMC on the expression of Bcl-2 protein and Bax protein. The antineoplastic activity and mechanism of action of BMC was explored comprehensively. The results showed that three new kinds of BMC (molar ratio of 2 : 1) were successfully prepared, the complexes molecular formula are: Na2Ni(C21H16O11)2 x 10H2O, Na2Co(C21H16O11)2 x 8H2O and Na2Cu(C21H16O11)2 x 8H2O. According to the results of cell cycle and apoptosis detection, BMC stopped cells at G0/G1 phase to S phase and G2/M phase. Gene and protein detection showed that under the given concentration and time, BMC can downregulate the expression of Bcl-2 gene in SMMC-7721 cells, and significantly decrease the expression of Bcl-2 protein, at the same time, with the increase of expression of Bax gene, the Bax protein's expression increased significantly. Which indicates that BMC restrain cell proliferation and cell apoptosis by stopping cell cycle, reducing the expression of Bcl-2 and increasing that of Bax; The anti-tumor activities of three kinds of complexes were: baicalin-copper (BC-Cu) > baicalin-cobalt (BC-Co) > baicalin-nickel (BC-Ni) > baicalin (BC), showing the dose-response relationship.

In this paper, the new carbon nanotube modified glassy carbon electrode (F-CNTs/GCE) was prepared to establish a new method for studying the molecular interaction mechanism between baicalin metal complexes (BMC) and bovine serum album (BSA), and the principle of this method was discussed deeply. Under the physiological condition, the thermodynamics and kinetics properties of interaction between BMC and BSA were studied by cyclic voltammetry (CV) to inference their molecular effective mechanism. The results show that the presence of F-CNTs can accelerate the electron transfer, and better response signal was showed in the BMC/BMC-BSA system. The detection of interaction of BMC-BSA used new method show that BMC-BSA generates stable thermodynamically non-covalent compounds, and the obtained average binding sites of BMC-BSA were 1.7; the number of electron transfer in BMC/BMC-BSA reaction process was 2, and non electroactive supramolecular compounds of BMC-BSA were generated by this interacting reaction. The relevant research work provides a new way to study the molecular mechanism for the interaction of drugs with protein, and with a certain reference value for discussion on the non covalent interactions.

BACKGROUND: Nowadays, stromal cell-derived factor-1 (SDF-1)/CXC chemokine receptor 4 (CXCR4) signal axis has been used extensively because of its biological effects and particularly a great progress has been achieved in the mechanism of SDF-1/CXCR4 signal axis as well as in its use for tissue regeneration. OBJECTIVE: To summarize the factors affecting the regulation of SDF-1 and CXCR4 and to review the research progress in the biological characteristics of SDF-1/CXCR4 signal axis. METHODS: The first author searched the PubMed, CNKI, WanFang and VIP databases for relevant articles published from January 1990 to August 2018. The keywords were "tissue engineering; cell homing; chemokine; regeneration; pulp regeneration; HIF-1; SDF-1; CXCL12; CXCR4; NOX-A12" in both Chinese and English. RESULTS AND CONCLUSION: Hypoxia-inducible factor-1 plays a key role in the regulation of SDF-1, and there are multiple factors which can affect the expression of CXCR4. SDF-1/CXCR4 signal axis formed by the combination of SDF-1 and CXCR4 plays an important biological role in various physiological and pathological processes. Blocking SDF-1 is used to inhibit the pathogenic effect of the SDF-1/CXCR4 signal axis for therapeutic purposes, while increasing SDF-1 can strengthen the SDF-1/CXCR4 signal axis and enhance the ability of chemotactic endogenous cell homing for tissue regeneration. To further illustrate the mechanism of the SDF-1/CXCR4 signal axis, we upregulate or downregulate the expression of SDF-1 or CXCR4 by exogenous means to influence the biological function of the signal axis, and thus provide theoretical basis for optimizing clinical treatment strategies, and developing the biological function of the signal axis for human health benefits.