The protective effect of Apelin-13 against cardiac hypertrophy through activating the PI3K-AKT-mTOR signaling pathway.

Objectives: To determine the protective effect of Apelin-13 on cardiac hypertrophy through activating the PI3K-AKT-mTOR signaling pathway. Materials and Methods: The phenylephrine-induced cardiomyocyte hypertrophy model was established in H9C2 cells in vitro. Electroporation transfection technology was utilized to prepare and screen the H9C2 cells inducing low expression of the angiotensin type one receptor-related protein (Si-APJ). H9C2 and Si-APJ cells were divided independently into five groups: the control group, the PE group, the PE+Apelin group, the PE+Rapa group, and the PE+Apelin+Rapa group. RT-PCR was performed to analyze the mRNA expression levels of myosin heavy chain 7 (MYH7). Expression of the PI3K/AKT/mTOR pathway proteins and MYH7 was investigated by western blot. Results: The expression of PI3K/AKT/mTOR phosphorylated proteins was significantly higher in the PE group compared with the PE+Apelin group in H9C2 cells (P<0.05). Conversely, in Si-APJ H9C2 cells, the expression of PI3K/AKT/mTOR phosphorylated proteins was decreased (P<0.05). In H9C2 cells, the expression of MYH7 protein was increased in the PE group compared with the control group (P<0.05). In the same cell line, the expression of MYH7 in the PE+Apelin group was decreased significantly compared with the PE group (P<0.05). In Si-APJ H9C2 cells, compared with the control group, the expression of MYH7 in the PE group still increased significantly (P<0.05). In contrast, in the same cell line, there was no statistically significant difference in MYH7 expression between the PE+Apelin, PE+Rapa, and PE+Apelin+Rapa groups compared to the PE group (P>0.05). Conclusion: Apelin-13 reduces PE-induced cardiac hypertrophy by activating the PI3K/AKT/mTOR signaling pathway.

Resveratrol inhibits matrix metalloproteinases-9 expression induced by soluble CD40 ligand in macrophages / 中华老年医学杂志

Objective To explore the effect of resveratrol on the expression of matrix metalloproteinases-9 (MMP-9) in soluble CD40 ligand (sCD40L)-activated macrophages. Methods Human monocytic cell line THP-1 cells under an inducing of phorbol ester differentiated into macrophages. Then the macrophages were sitimulated by sCD40L independently and after a preincubation with resveratrol. The mRNA expression of MMP-9 and tissue-inhibitor of metalloproteinase-1 (TIMP-1) in macrophages were investigated by semiquantitative RT-PCR. The secretions of MMP-9 and TIMP-1 protein were measured by Western blot. The MMP-9 activity was analyzed by gelatin zymography technique. Results The expressions of MMP-9 gene(1.53±0.04 vs. 0.75±0.01,P＜0.05) and protein(244 930.8±31 268.6 vs. 192 976.8±20 223.1,P＜0.05)were higher in macrophages when stimulated by sCD40L. Resveratrol (10 μmol/L and 50 μmol/L)can inhibit the CD40L-induced gene expression and the protein secretion of MMP-9 (P＜0.01). The activity of MMP-9 was degraded by resveratrol (P＜0.05). Meanwhile resveratrol could increase the gene expression and protein secretion of TIMP-1 (P＜0.05). Conclusions Resveratrol can inhibit the CD40L-activated macrophage expression of MMP-9. It may be one of its mechanisms on antiatherosclerosis and stabilization of atheromatous plaques.

Effects of resveratrol on the expressions of E-selectin and monocyte chemoattractant protein-1 of endothelial cells / 中华老年医学杂志

ObjectiveTo investigate the effect of resveratrol on the expressions of E-selectin and monocyte chemoattractant protein-1 (MCP-1) in activated endothelial cells.Methods After being pretreated with resveratrol followed by tumor necrosis factor-α (TNF-α) stimulation, human umbilical vein endothelial cells (HUVEC) were randomly divided into three groups: TNF group,resveratrol+TNF-α group and control group. The expression of E-selectin molecule on the surface of HUVEC was detected by flow cytometric analysis and the mRNA expressions of E-selectin and MCP -1 were determined by semiquantitative RT-PCR. ResultsTNF-α induced the expression of E-selectin and MCP-I of HUVEC.Resveratrol (10 μmol/L) inhibited E-selectin expression.The positive cells of E-selectin in TNF group, resveratrol + TNF-α group and control group were(47.84±3.2)%, (15.3±1.7)% and (3.74±1.6)%, respectively, and the differences among the three groups were statistically significant (P<0.05). Conclusions Resveratrol may contribute to the anti-atherosclerotic effect by inhibiting the expression of E-seleetin and MCP-1 of HUVEC.

Resveratrol Attenuated Reactive Oxygen Species in Injured Endothelial Cells / 中华高血压杂志

Background Resveratrol has been unanimously recognized as an cardiovascular protective substance in red wine. It has been speculated that the anti-atherosclerosis effect of resveratrol is ascribed to its powerful anti-inflammatory effect. Objective To investigate the effects of resveratrol on injured human umbilical veno-endothelial cells (HUVEC) and the reactive oxygen species(ROS) production induced by TNF-? or soluble CD40L (sCD40L). Methods Cultured HUVEC were pre-incubated with resveratrol(1-50 ?mol/L) for 2 hours and then treated with TNF-?(10 ?g/L) or sCD40L?(10 ?g/L) for another 4 hours. MTT assay was used to detect proliterative activity of HUVEC. Immunofluorescence microscopy was used for determination of ROS expression. Results Both TNF-? and sCD40L impaired HUVEC proliferation (-32.7% and -26% vs control,P