Objective To investigate the effect of lycopene (Lyc) on H9c2 cell apoptosis induced by angiotensin Ⅱ (Ang Ⅱ).Methods Using Ang Ⅱ (10 μmol/L) to stimulate H9c2 cells,we observed the protective effect of Lyc on H9c2 cells apoptosis.The H9c2 cells viability induced by different consideration of Lyc or Ang Ⅱ or both was detected by CCK8 assay.The expression levels of Bax and Bcl-2 in H9c2 cells were determined by real-time quantitative reverse transcription polymerase chain reaction (RT-PCR).Western blot was conducted to detect the protein expressions of Bax,Caspase 3,Caspase 9 and Bcl-2 in H9c2 cells.The apoptotic ratio of H9c2 cells was observed by TUNEL assay.Results Compared with control group,Ang Ⅱ could decrease the viability of H9c2 cells to (92.87±4.37)％.The result of RT-PCR showed that Ang Ⅱ decreased the expression level of Bcl-2,and Bax level was increased under the stimulation of Ang Ⅱ (P＜0.05),while the expression level of Bcl-2 was increased and Bax level was decreased under the co-stimulation of Ang Ⅱ and Lyc in a concentration dependent manner,which indicated that Lyc ameliorated the apoptosis of H9c2 cells.The result of western blot showed that the protein expressions of Bax,Caspase 3 and Caspase 9 were increased,but Bcl-2 was decreased after the stimulation of Ang Ⅱ (P＜0.05).While these phenomenon reversed apparently under the co stimulation of Ang Ⅱ and Lyc.A large number of apoptotic cells were observed under the stimulation of Ang Ⅱ through TUNEL assay.But the number of apoptotic cells reduced significantly under the co-stimulation of Lyc and Ang Ⅱ (P ＜0.05).Conclusions Lyc ameliorates the H9c2 cell apoptosis induced by Ang Ⅱ,which indicates that Lyc may have an important role in the treatment of various cardiovascular diseases.

Objective To investigate the effect of Lycopene (Lyc) on Ang Ⅱ induced oxidative stress in H9c2 cell line derived from rat cardiac tissue,and to explore related mechanisms.Methods H9c2 cells were divided into 6 groups:control group,Ang Ⅱ group (1 μmol/L),Ang Ⅱ (1 μmol/L) + low dose Lyc (3.125 nmol/L) group,AngⅡ (1 μmol/L) + moderate dose Lyc(6.25 nmol/L)group and Ang Ⅱ (1 μmol/L) + high dose Lyc(12.5 nmol/L) group and Lyc group (12.5 nnmol/L).Cell growth was determined by CCK8 assay,ROS generation was detected using a Microplate reader and Fluorescence microscopy,the expression of NOX2 was determined by Western blot,mRNA expression of p47phox,SOD1 and SOD2 were determined by Real Time-PCR,MDA was detected by ELISA kit.Results Compared to control group,cell survival was significantly reduced and ROS generation was significantly increased post Ang Ⅱ stimulation,cotreatment with Lyc significantly improved cell survival and reduced ROS generation in a dosedependent manner (all P ＜ 0.01).mRNA expression of SOD1 and SOD2 was significantly downregulated while MDA concentration was significantly increased in Ang Ⅱ treated cells,which could be significantly reversed by cotreatment with Lyc in a dose dependent manner (all P ＜ 0.01).Protein expression of NOX2 and mRNA expression of p47phox were significantly upregulated post Ang Ⅱ and which could be significantly downregulated by cotreatment with Lyc in a dose-dependent manner (all P ＜ 0.01).Conclusion Lyc could attenuate Ang Ⅱ induced oxidative stress and this effect is linked with its capacity of reducing ROS generation and enhancing cellular ROS scavenging ability in H9c2 cells.

Abstract： ObjectiveThe study aims to explore the effects and regulatory roles of glucose transporter 1 （GLUT1） on the proliferation， migration， adhesion， and angiogenesis of human umbilical vein endothelial cells （HUVECs） under ischemia-hypoxic conditions. MethodsIn vitro experiments were conducted to subject HUVECs to an ischemia-hypoxic-mimicking environment （1% O₂， 5% CO₂， 94% N₂）. The biological characteristics of HUVECs under normoxic and ischemia-hypoxic conditions were compared by assessing cell viability， proliferation capacity， and examining the expression changes of GLUT1， HIF-1α， and VEGFA proteins under ischemia-hypoxia using Western blot technology. Further， GLUT1 was overexpressed using plasmid transfection and the proliferation， migration， adhesion， and angiogenic capabilities of HUVECs were evaluated through scratch assays， cell adhesion assays， and tube formation assays. Mitochondrial morphological changes were observed by transmission electron microscopy，and oxygen consumption rate （OCR） was detected by Seahorse metabolic analyzer to evaluate mitochondrial function. ResultsCompared with normoxic conditions， the ischemia-hypoxic environment significantly inhibited the proliferation， cell viability， migration， and adhesion capabilities of HUVECs and impaired their angiogenic potential. The expression levels of GLUT1， HIF-1α and VEGFA proteins were also markedly reduced. However， when GLUT1 expression was upregulated， the migration， adhesion， and angiogenic capabilities of HUVECs were significantly improved， and the protein expression levels of HIF-1α， VEGFA and VEGFR were increased. Transmission electron microscopy revealed that ischemic-hypoxia leads to mitochondrial swelling and matrix damage， while GLUT1 overexpression significantly alleviates mitochondrial morphology abnormalities. OCR results suggest that GLUT1 overexpression may enhance oxidative phosphorylation of endothelial cells in ischemic-hypoxic environments to improve energy metabolism. These results suggest that GLUT1 may influence the function and angiogenic potential of HUVECs by regulating glucose metabolism and energy supply. ConclusionsThis study reveals the significant regulatory role of GLUT1 in the function of HUVECs under ischemia-hypoxic conditions， potentially through modulating cellular energy metabolism and signal transduction pathways， thereby affecting cell proliferation， migration， adhesion， and angiogenesis. These findings provide a new perspective on the role of GLUT1 in cardiovascular diseases and may offer potential targets for the development of new therapeutic strategies.