scholarly journals Anticancer Activity of Polysaccharides Produced from Glycerol and Crude Glycerol by an Endophytic Fungus Chaetomium globosum CGMCC 6882 on Human Lung Cancer A549 Cells

Biomolecules ◽  
2018 ◽  
Vol 8 (4) ◽  
pp. 171 ◽  
Author(s):  
Zichao Wang ◽  
Peizhang Chen ◽  
Ning Tao ◽  
Huiru Zhang ◽  
Ruifang Li ◽  
...  
Keyword(s):  
Crude Glycerol ◽  
Caspase 3 ◽  
A549 Cells ◽  
Biodiesel Production ◽  
Chaetomium Globosum ◽  
Human Lung Cancer ◽  
Control Group ◽  
Rt Pcr ◽  
Caspase 9 ◽  
Molecular Weights

Two polysaccharides were produced by Chaetomium globosum CGMCC 6882 from glycerol (GCP-1) and crude glycerol (GCP-2). Chemical characteristics results showed GCP-1 and GCP-2 were similar polysaccharides, but the molecular weights of GCP-1 and GCP-2 were 5.340 × 104 Da and 3.105 × 104 Da, respectively. Viabilities of A549 cells after treatment with GCP-1 and GCP-2 were 49% and 39% compared to the control group. Meanwhile, flow cytometry results indicated that GCP-1 and GCP-2 could induce 17.79% and 24.28% of A549 cells to apoptosis with 200 μg/mL concentration treated for 24 h. RT-PCR results suggested that GCP-1 and GCP-2 could be used as potential and effective apoptosis inducers on A549 cells by increasing BAX, CASPASE-3, CASPASE-9, TIMP-1, TIMP-2 expression and decreasing BCL-2 expression. This research provided an innovative approach to using a byproduct of biodiesel production (crude glycerol) to produce polysaccharides of potential medicinal benefit.

Inhibitory effect of lignans from Ailanthus altissima on proliferation of human lung cancer cells and its mechanism.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e15059-e15059
Author(s):  
Yu Wang ◽  
Siming Wang ◽  
Yibing Wu ◽  
Mei Dong ◽  
Zhiyu Ni
Keyword(s):  
Lung Cancer ◽  
Caspase 3 ◽  
Human Lung ◽  
A549 Cells ◽  
Inhibitory Effect ◽  
Human Lung Cancer ◽  
Ailanthus Altissima ◽  
Control Group ◽  
Caspase Inhibitor ◽  
Significant Difference

e15059 Background: Plants are thought to contain compounds that inhibit the proliferation of cancer cells in vitro, and many attempts have been made to isolate anti-cancer drugs from plants. Ailanthus altissima is a family of Simaroubaceae, the bark is gray to grayish-black, because of the smell of the gland patches at the base of the leaves. 3,5,3-trimethoxy-8,1-neoligna-4,2,7,9,9-pentol (TNP) isolated from Ailanthus altissima. Methods: (1) Apoptosis was detected by flow cytometry: the cells were incubated with 10 mmol/L TNP for 24 h, and the cells were collected. The cell concentration was adjusted to 5×105 ̃ 5×106/ L. While propionate iodide was added for DNA fluorescence staining (Propidium Iodide, PI: 50 mg/L，triton-x100 1.0%). (2) The changes of p53, Bax and caspase-3 were detected by Western blot. The cells were cultured in 10 μmol/L cisplatin and TNP medium for 24 hours. Image J image analysis software is used for semi quantitative analysis. The data were expressed by mean standard deviation, and the mean values of each group were compared by analysis of variance and the least significant difference. There was a significant difference in P< 0.05. (3) A549 cells were treated with 10 μmol/L cisplatin and TNP. A549 cells were incubated with cisplatin and TNP, and then treated with solvent control (final concentration 0.1% dimethyl sulfoxide) with or without caspase inhibitor for 48 hours The OD value was determined by MTT method. Cell survival rate (%) = (OD value of control group /OD value of control group) 100%. Results: (1) The reverse effect of caspase inhibitor on the proliferation of A549 cells: the cell survival rates of A549 cells treated with 0.1, 1 and 10 μmol/L cisplatin and TNP were 96.11%, 72.36%, 27.57% and 71.42%, 28.97% and 4.34% respectively. The survival rate of A549 cells incubated with cisplatin and TNP 20 μmol/L increased to 100.00%, 81.92%, 57.54% and 85.69%, 48.57% and 16.95% respectively. Caspase inhibitor reversed the inhibitory effect of TNP on A549 cells. (2) The effect of TNP on apoptosis of A549 cells: after treatment with 10 μmol/L TNP for 24 h, the apoptosis rate of A549 cells was (24.01)%, which was significantly higher than that of the blank control group (6.79)% ( P< 0.05). (3) The results showed that the up regulation of p53, Bax and caspase-3 protein by TNP was 10 μmol/L. Conclusions: TNP can induce apoptosis of human lung cancer cell line A549, and it can up regulate the expression of p53, Bax and Caspase-3, which may be one of the mechanisms of TNP inducing apoptosis of A549 cells. The experiment also proves that caspase inhibitor can reverse the effect of TNP. TNP inhibits the proliferation of A549 cells.

scholarly journals Lotus leaf flavonoids induce apoptosis of human lung cancer A549 cells through the ROS/p38 MAPK pathway

2021 ◽  
Vol 54 (1) ◽  
Author(s):  
Xiang-Bo Jia ◽  
Quan Zhang ◽  
Lei Xu ◽  
Wen-Jian Yao ◽  
Li Wei
Keyword(s):  
Lung Cancer ◽  
P38 Mapk ◽  
Caspase 3 ◽  
Human Lung ◽  
Mapk Pathway ◽  
A549 Cells ◽  
Human Lung Cancer ◽  
Caspase 9 ◽  
Lotus Leaf

Abstract Background Leaves of the natural plant lotus are used in traditional Chinese medicine and tea production. They are rich in flavonoids. Methods In this study, lotus leaf flavonoids (LLF) were applied to human lung cancer A549 cells and human small cell lung cancer cells H446 in vitro to verify the effect of LLF on apoptosis in these cells through the ROS/p38 MAPK pathway. Results LLF had no toxic effect on normal cells at concentrations up to 500 µg/mL, but could significantly inhibit the proliferation of A549 cells and H446 cells. Flow cytometry showed that LLF could induce growth in A549 cells. We also found that LLF could increase ROS and MDA levels, and decrease SOD activity in A549 cells. Furthermore, qRT-PCR and western blot analyses showed that LLF could upregulate the expression of p38 MAPK (p-p38 MAPK), caspase-3, caspase-9, cleaved caspase-3, cleaved caspase-9 and Bax and downregulate the expression of Cu/Zn SOD, CAT, Nrf2, NQO1, HO-1, and Bcl-2 in A549 cells. Results of HPLC showed that LLF mainly contain five active substances: kaempferitrin, hyperoside, astragalin, phloridzin, and quercetin. The apoptosis-inducing effect of LLF on A549 cells came from these naturally active compounds. Conclusions We have shown in this study that LLF is a bioactive substance that can induce apoptosis in A549 cells in vitro, and merits further research and development.

Brucea javanica Oil Induces Apoptosis in T24 Bladder Cancer Cells via Upregulation of Caspase-3, Caspase-9, and Inhibition of NF-κB and COX-2 Expressions

2010 ◽  
Vol 38 (03) ◽  
pp. 613-624 ◽  
Author(s):  
Guo-Guang Lou ◽  
Hang-Ping Yao ◽  
Li-Ping Xie
Keyword(s):  
Caspase 3 ◽  
Flow Cytometric Analysis ◽  
Morphological Characteristics ◽  
Control Group ◽  
Caspase 9 ◽  
Brucea Javanica ◽  
Flow Cytometric ◽  
T24 Cells ◽  
Bladder Cancer Cells ◽  
Cox 2

The potential molecular mechanism of Brucea javanica oil in the induction of apoptosis of T24 bladder cancer cells was investigated in vitro. T24 cells were divided into two groups: one, treated with B. javanica oil and the other, untreated. The cells were maintained in Dulbecco's modified Eagle's medium (DMEM) containing 10% fetal calf serum (FCS) and 4 mM glutamine. The morphological characteristics of T24 cells were examined microscopically at the 2nd and 5th day of the culture. The drug toxicity spectrum ( IC 50) was estimated by the MTT assay, and viability of T24 cells was assessed on the basis of the percentage of T24 apoptotic cells, as determined by Annexin/PI staining and flow cytometric analysis. The expression of caspase-3, capase-9, NF-κB p65, and COX-2 was analyzed by Western blotting. Morphological characteristics of the cells on the 2nd day showed apoptosis of the treated T24 cells; it was more apparent in the cells on the 5th day. B. javanica oil decreased the cell viability at the testing concentrations spectrum (5–0.156 mg/ml), and this viability was significantly higher as compared to the control group. In this concentration spectrum, B. javanica oil also induced apoptosis of T24 cells, which was analyzed by annexin/PI staining and flow cytometric analysis. These results were also statistically significant as compared to those of the control group. The expressions of caspase-3 and caspase-9 were low in the control T24 cells, while the expressions of NF-κB and COX-2 were high in normal T24 cells. Treatment with B. javanica oil significantly induced the expressions of caspase-3 and caspase-9 proteins in T24 cells, whereas the expressions of NF-κB and COX-2 proteins were inhibited. B. javanica oil significantly reduced the viability of T24 cells and induced T24 cell apoptosis. The molecular mechanism underlying these effects may be the activation of caspase apoptotic pathway by upregulation of the expression of caspase-3 and caspase-9 proteins and inhibition of the expression of NF-κB and COX-2 proteins.

scholarly journals Silica nanoparticles inducing the apoptosis of spermatocyte cell through microRNA-450b-3p targeting MTCH2-mediating mitochondrial signaling pathway

2020 ◽  
Author(s):  
Guiqing Zhou ◽  
Jianhui Liu ◽  
Xiangyang Li ◽  
Yujian Sang ◽  
Yue Zhang ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Silica Nanoparticles ◽  
Caspase 3 ◽  
Reproductive Toxicity ◽  
Control Group ◽  
Caspase 9 ◽  
Protein Expressions ◽  
Underlying Mechanisms

Abstract Background: Silica nanoparticles (SiNPs) are found in environmental particulate matter and are proven to have adverse effects on fertility. The relationship and underlying mechanisms between miRNAs and apoptosis induced by SiNPs during spermatogenesis is currently ambiguous. Experimental design: The present study was designed to investigate the role of miRNA-450b-3p in the reproductive toxicity caused by SiNPs. In vivo, 40 male mice were randomly divided into control and SiNPs groups, 20 per group. The mice in the SiNPs group were administrated 20 mg/kg SiNPs by tracheal perfusion once every 5 days, for 35 days, and the control group were given the equivalent of a normal luminal saline. In vitro, spermatocyte cells were divided into 0 and 5 μg/mL SiNPs groups, after passaged for 30 generations, the GC-2spd cells in 5 μg/mL SiNPs groups were transfected with miRNA-450b-3p and its mimic and inhibitor. Results: In vivo, the results showed that SiNPs damaged tissue structures of testis, decreased the quantity and quality of the sperm, reduced the expression of miR-450b-3p, and increased the protein expressions of the MTCH2, BID, BAX, Cytochrome C, Caspase-9, and Caspase-3 in the testis. In vitro, SiNPs obviously repressed the viability and increased the LDH level and apoptosis rate, decreased the levels of the miR-450b-3p, significantly enhanced the protein expressions of the MTCH2, BID, BAX, Cytochrome C, Caspase-9, Caspase-3; while the mimic of miR-450b-3p reversed the changes induced by SiNPs, but inhibitor further promoted the effects induced by SiNPs.Conclusion: The result suggested that SiNPs could induce the spermatocyte apoptosis by inhibiting the miR-450b-3p expression to target promoting the MTCH2 resulting in activating mitochondrial apoptotic signaling pathways in the spermatocyte cells.

Hydroxychloroquine Blocks Autophagy and Promotes Apoptosis of the Prostate after Castration in Rats

2020 ◽  
Vol 104 (11-12) ◽  
pp. 968-974
Author(s):  
Sheng-Tao Ling ◽  
Chun-Lei Deng ◽  
Li Huang ◽  
Qi-Sheng Yao ◽  
Cui Liu ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Morphological Changes ◽  
Control Group ◽  
Sham Operation ◽  
Related Gene ◽  
Rt Pcr ◽  
Bax Protein ◽  
Sd Rats ◽  
Immunohistochemical Analyses ◽  
Scanning Electron

Autophagy is an important pro-survival mechanism and closely related to apoptosis. The aim of this study was to investigate whether hydroxychloroquine (HCQ) blocks autophagy and promotes apoptosis of the prostate after castration. <b><i>Methods:</i></b> Thirty-six male SD rats were randomly divided into 3 groups (<i>n</i> = 12): control group (sham operation), castration group, and HCQ group (castrated and treated with HCQ). On day 7, all mice were executed and prostates were isolated. The morphological changes of prostates were observed by light microscope, and the ultrastructure changes were observed under scanning electron microscope (SEM). The protein expression of Beclin-l, P62, caspase-3, Bcl-2, and Bax was assessed by immunohistochemical analyses. The mRNA expression of microtubule-associated protein light chain 3 (LC3) and autophagy-related gene 5 (Atg5) was detected by RT-PCR. <b><i>Results:</i></b> Prostates of castration group shrank remarkably and prostates of HCQ group shrank more remarkably than castration group. Cytolysosomes were visible in the prostates of the castration group under SEM. Immunohistochemistry showed that the protein of Beclin-1 increased in the castration group compared to the control group, while decreased in the HCQ group compared to the castration group. While P62 protein moderately dyed in the control group and weakly dyed in the castration group, it strongly dyed in the HCQ group. Caspase-3 and Bax protein were weakly dyed in the control group but moderately dyed in the castration group and strongly dyed in the HCQ group. The expressions of apoptosis suppressor Bcl-2 were reduced in the castration group and further reduced in the HCQ group compared to the castration group. RT-PCR revealed that the mRNA of LC3 and Atg5 in the castration group increased compared to the control group, while decreased after treated with HCQ. <b><i>Conclusion:</i></b> Autophagy increased after castrated in prostates, while decreased after treated with HCQ; all these indicated that HCQ blocked autophagy and then promoted prostate apoptosis of castrated mice.

Effects of 5,6-Dihydroxy-2,4-Dimethoxy-9,10-Dihydrophenanthrene on G2/M Cell Cycle Arrest and Apoptosis in Human Lung Carcinoma Cells

2016 ◽  
Vol 44 (07) ◽  
pp. 1473-1490 ◽  
Author(s):  
Wipada Duangprompo ◽  
Kalaya Aree ◽  
Arunporn Itharat ◽  
Pintusorn Hansakul
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Caspase 3 ◽  
Human Lung ◽  
A549 Cells ◽  
Human Lung Cancer ◽  
Apoptotic Cells ◽  
Mrna Levels ◽  
Cycle Arrest

5,6-dihydroxy-2,4-dimethoxy-9,10-dihydrophenanthrene (HMP) is an active compound isolated from the rhizome extracts of Dioscorea membranacea Pierre, a Thai medicinal plant. This study aimed to investigate the growth-inhibitory and apoptosis-inducing effects of HMP in human lung cancer A549 cells. The antiproliferative and cytotoxic effects of HMP were analyzed by a Sulforhodamine B assay. Cell division, cell cycle distribution and membrane asymmetry changes were each performed with different fluorescent dyes and then analyzed by flow cytometry. Real-time PCR and immunoblotting were used to detect cell cycle- and apoptosis-related mRNA levels and proteins, respectively. The nuclear morphology of the cells stained with DAPI and DNA fragmentation were detected by fluorescence microscopy and gel electrophoresis, respectively. The results showed that HMP exerted strong antiproliferative and cytotoxic activities in A549 cells with the highest selectivity index. It halted the cell cycle in [Formula: see text]/M phase via down-regulation of the expression levels of regulatory proteins Cdc25C, Cdk1 and cyclinB1. In addition, HMP induced early apoptotic cells with externalized phosphatidylserine and subsequent apoptotic cells in sub-[Formula: see text] phase. HMP increased caspase-3 activity and levels of the cleaved (active) form of caspase-3 whose actions were supported by the cleavage of its target PARP, nuclear condensation and DNA apoptotic ladder. Moreover, HMP significantly increased the mRNA and protein levels of proapoptotic Bax as well as promoted subsequent caspase-9 activation and BID cleavage, indicating HMP-induced apoptosis via both intrinsic and extrinsic pathways. These data support, for the first time, the potential role of HMP as a cell-cycle arrest and apoptosis-inducing agent for lung cancer treatment.

Overexpression of Smac Promotes Cisplatin-Induced Apoptosis by Activating Caspase-3 and Caspase-9 in Lung Cancer A549 Cells

2013 ◽  
Vol 28 (2) ◽  
pp. 177-182 ◽  
Author(s):  
Sida Qin ◽  
Chengcheng Yang ◽  
Xifang Wang ◽  
Chongwen Xu ◽  
Shuo Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Caspase 3 ◽  
A549 Cells ◽  
Caspase 9 ◽  
Induced Apoptosis

scholarly journals The mitochondrial calcium uniporter induces apoptosis in cardiomyocytes cultured with high-glucose medium by affecting mitochondrial function

2020 ◽  
Author(s):  
Xia Chen ◽  
Wenyun Guo ◽  
Zhe Jing ◽  
Tao Zhang ◽  
Zhaoqi Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
Caspase 3 ◽  
Normal Group ◽  
Control Group ◽  
Caspase 9 ◽  
Mitochondrial Ros ◽  
H9c2 Cardiomyocytes ◽  
Experimental Group

Abstract Background As the number of diabetics worldwide continues to increase, diabetic cardiomyopathy has become one of the main causes of cardiovascular disease risk in diabetic patients. Currently, the pathophysiological mechanism of DCM has not been fully elucidated. In the present study, relevant pathological changes of cardiomyocytes in the high glucose environment were simulated by in vitro culture of rat H9C2 cardiomyocytes, to explore the mechanism by which MCU induces apoptosis in cardiomyocytes. Method: Cultured rat myocardium H9C2 cells in vitro and divided into high glucose group (glucose concentration 33 mmol/L), normal group (glucose concentration 5.5 mmol/L), experimental group (5.5 mmol/L glucose and transfected with MCU siRNA) and control group (5.5 mmol/L glucose and transfected negative control siRNA). Comparative analysis of MCU expression, Ca2+ uptake, mitochondrial function, oxidative stress and apoptosis of two groups of cells. Results (1) Compared with normal group, in the high glucose group the MCU expression of myocardial cells in H9C2 rats decreased, The Ca2+ levels, membrane potential and mitochondrial ATP levels decreased, mitochondrial ROS levels increased, NADH+/NADPH ratio in cardiomyocytes increased, GSH/GSSG ratio decreased, the expression levels of cleaved caspase-3 and cleaved caspase-9 increased, bcl-2 expression decreased, the number of cardiomyocytes apoptotic cells increases. (2) Compared with the normal group and the control group, the experimental group MCU expression of myocardial cells in H9C2 rats decreased, The Ca2+ levels, membrane potential and mitochondrial ATP levels decreased, mitochondrial ROS levels increased, NADH+/NADPH ratio in cardiomyocytes increased, GSH/GSSG ratio decreased, the expression levels of cleaved caspase-3 and cleaved caspase-9 increased, bcl-2 expression decreased, the number of cardiomyocytes apoptotic cells increases. Discussion This study suggested that MCU expression in rat H9C2 cardiomyocytes was decreased in the high glucose environment, causing abnormal mitochondrial calcium uptake and imbalanced calcium homeostasis, which may further contribute to mitochondrial dysfunction and enhanced oxidative stress in cardiomyocytes. Mitochondrial dysfunction and enhanced oxidative stress ultimately led to apoptosis in cardiomyocytes.

scholarly journals Neuroinflammation trajectories precede cognitive impairment after experimental meningitis—evidence from an in vivo PET study

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Vijayasree V. Giridharan ◽  
Allan Collodel ◽  
Jaqueline S. Generoso ◽  
Giselli Scaini ◽  
Rico Wassather ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Microglial Activation ◽  
Caspase 3 ◽  
Cns Infection ◽  
Control Group ◽  
Caspase 9 ◽  
Activation Markers

Abstract Background Bacterial meningitis is a devastating central nervous system (CNS) infection with acute and long-term neurological consequences, including cognitive impairment. The aim of this study was to understand the association between activated microglia-induced neuroinflammation and post-meningitis cognitive impairment. Method Meningitis was induced in male Wistar rats by injecting Streptococcus pneumoniae into the brain through the cisterna magna, and rats were then treated with ceftriaxone. Twenty-four hours and 10 days after meningitis induction, rats were imaged with positron emission tomography (PET) using [11C]PBR28, a specific translocator protein (TSPO) radiotracer, to determine in vivo microglial activation. Following imaging, the expression of TSPO, cardiolipin, and cytochrome c, inflammatory mediators, oxidative stress markers, and glial activation markers were evaluated in the prefrontal cortex and hippocampus. Ten days after meningitis induction, animals were subjected to behavioral tests, such as the open-field, step-down inhibitory avoidance, and novel object recognition tests. Results Both 24-h (acute) and 10-day (long-term) groups of rats demonstrated increased [11C]PBR28 uptake and microglial activation in the whole brain compared to levels in the control group. Although free from infection, 10-day group rats exhibited increased expression levels of cytokines and markers of oxidative stress, microglial activation (IBA-1), and astrocyte activation (GFAP) similar to those seen in the 24-h group. Acute meningitis induction also elevated TSPO, cytochrome c, and caspase-3 levels with no change in caspase-9 levels. Furthermore, upregulated levels of TSPO, cytochrome c, and caspase-3 and caspase-9 were observed in the rat hippocampus 10 days after meningitis induction with a simultaneous reduction in cardiolipin levels. Animals showed a cognitive decline in all tasks compared with the control group, and this impairment may be at least partially mediated by activating a glia-mediated immune response and upregulating TSPO. Conclusions TSPO-PET could potentially be used as an imaging biomarker for microglial activation and long-term cognitive impairment post-meningitis. Additionally, this study opens a new avenue for the potential use of TSPO ligands after infection-induced neurological sequelae.

scholarly journals JNK pathway promotes hepatocyte apoptosis by inhibiting Bcl-2 and upregulating expressions of Bim, caspase-3 and caspase-9 after cardiopulmonary bypass

2020 ◽  
Vol 19 (3) ◽  
pp. 519-524
Author(s):  
Haibin Yu ◽  
Haojie Zhang ◽  
Yan Cheng ◽  
Xian’en Fa ◽  
Fangtao Zhu ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Protein Expression ◽  
Caspase 3 ◽  
Control Group ◽  
Hepatocyte Apoptosis ◽  
Caspase 9 ◽  
Jnk Pathway ◽  
Expression Levels ◽  
Over Expression ◽  
Mrna Expression Levels

Purpose: To study the effect of Jun N-terminal kinase (JNK) signaling pathway on hepatocyte apoptosis in vivo and in vitro, and to elucidate the mechanism of action. Methods: TdT-mediated dUTP Nick-End Labeling (TUNEL) method was used to determine apoptosis in control and cardiopulmonary bypass (CPB) groups at 0, 3 and 6 hours after rat surgery. The expressions of JNK and p-c-Jun in liver tissues at 0, 3 and 6 h after surgery, and the levels of p-c-Jun, Bcl-2 and Bim following overexpression of JNK, were determined using Western blot assay. Human liver cell line HL-7702 was cultured and transfected with over-expressed JNK plasmid and empty plasmid. Proliferation of HL-7702 cells after JNK over-expression was assessed by Cell Counting Kit-8 (CCK-8), while quantitative real-time polymerase chain reaction (RT-qPCR) was employed to evaluate mRNA expression levels of caspase-3 and caspase-9 mRNA after JNK over-expression. Apoptosis of the cells was determined by flow cytometry (FC) after JNK over-expression. Results: FC results showed that the number of apoptotic hepatocytes increased after JNK overexpression in hepatocytes while TUNEL assay results demonstrated that hepatocyte apoptosis increased in CPB group, when compared to control group; furthermore, the number of apoptotic cells gradually increased within 6 h after surgery. The expressions of JNK and p-c-Jun were higher in CPB group than in control group, and increased gradually in both groups within 6 h after surgery. Overexpression of JNK decreased the proliferation of hepatocytes, and also lowered protein expression levels of p-c-Jun and Bim; on the other hand, the protein expression levels of Bcl-2 fell, while mRNA expression levels of caspase-3 and caspase-9 mRNA increased. Conclusion: JNK pathway promotes hepatocyte apoptosis after cardiopulmonary bypass by inhibiting Bcl-2 pathway and promoting the expressions of Bim caspase-3 and caspase-9. Keywords: Cardiopulmonary bypass, Apoptosis, JNK pathway, Bim, caspase-3 and caspase-9

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