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.

The T-Box transcription factor family plays a crucial role during heart development. A large amount of clinical evidence showed TBX 1, 2, 5, 18, 20 proteins to be strongly associated with human congenital heart diseases including atrial septal defect, mitral valve disease, and tetralogy of Fallot. Among these, TBX20 has attracted much attention. This article gives a brief review for the progress made in the research on TBX20 and cardiovascular disease.
Cardiovascular Diseases ; prevention & control ; Gene Expression Regulation ; Humans ; T-Box Domain Proteins ; genetics

OBJECTIVETo 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.

METHODSH9c2 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, Ang II (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 p47(phox), SOD1 and SOD2 were determined by Real Time-PCR, MDA was detected by ELISA kit.

RESULTSCompared 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 dose-dependent 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 p47(phox) 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).

CONCLUSIONLyc 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.

Angiotensin II ; Animals ; Carotenoids ; pharmacology ; Cell Line ; Cell Proliferation ; Cell Survival ; Cells, Cultured ; Down-Regulation ; Heart ; Oxidative Stress ; RNA, Messenger ; Rats ; Reactive Oxygen Species ; metabolism ; Up-Regulation