ABSTRACT
OBJECTIVE To investigate the effects and mechanism of luteolin on osteogenic repair of bone defects. METHODS The targets and potential pathways of luteolin in the treatment of bone defects were screened by network pharmacology method， and then the top 2 targets were selected by Hub gene screening for molecular docking verification， with binding energy as the evaluation standard. In vitro experiments were conducted on rat bone mesenchymal stem cells （BMSC） and rat umbilical vein endothelial cells （RUVEC）. Phenotypic validation was performed using alkaline phosphatase staining， alizarin red S staining， and in vitro angiogenesis experiments. Western blot assay was used to detect the protein expressions of phosphatidylinositol 3 kinase （PI3K） and protein kinase 1 （Akt1）， so as to validate the mechanism of luteolin on osteogenic differentiation of BMSC and angiogenesis of RUVEC in vitro. RESULTS The results of network pharmacology showed that the effects of luteolin on vascular formation and bone repair in bone defects were mainly related to Akt1， SRC， estrogen receptor 1， epidermal growth factor receptor， cyclooxygenase 2， matrix metalloproteinase 9 targets， and were closely related to PI3K-Akt signaling pathway. The results of molecular docking showed that luteolin binding to Akt1 and SRC proteins was stable. The results of in vitro experiments showed that luteolin could significantly improve the expressions and activities of alkaline phosphatase in BMSC， increased the number of calcium salt deposits and calcified nodules， and promoted calcification of BMSC. Compared with luteolin 0 μmol/L group， the angiogenesis ability of RUVEC was enhanced significantly in luteolin 1， 10 μmol/L groups， the length of blood vessels and the protein expressions of PI3K and Akt1 were significantly increased （P＜0.05 or P＜0.01）； the higherthe concentration， the better the effect. CONCLUSIONS Luteolin may play a role in promoting angiogenesis and bone repair at the fracture site by activating PI3K/Akt signaling pathway and promoting the protein expressions of PI3K and Akt1.
ABSTRACT
Objective To investigate the change and clinical value of serum cystain C(CysC)level in the patients with HBeAg-negative chronic hepatitis B(CHB).Methods 212 cases of CHB in our hospital were selected and divided into the HBeAg-negative group and the HBeAg-positive group according to the HBeAg status.105 healthy individuals at the same time were enrolled as the control group.The levels of serum CysC,ALT,AST,Cr,BUN and HBV DNA in 3 groups were detected and compared.The corre-lations between serum CysC with AST,AST,Cr,Bun,HBV DNA were analyzed by the Pearson correlation analysis.Results The mean CysC level in the HBeAg-negative group was (1 .40±0.36)mg/L,which was higher than (0.93±0.12)mg/L in the control group and (0.96±0.18)mg/L in the HBeAg-positive group,the differences between them was statistically significant(P <0.05). The CysC was significantly positively correlated with serum Cr level in the HBeAg-negative group(r=0.840,P <0.01).Conclusion The CysC level might be used as an effective index for monitoring the early kidney injury in the patients with HBeAg-negative CHB,which has important significance in the prevention and treatment of HBeAg-negative CHB.