Objective To explore the protective role and mechanisms of glucagon-like peptide-1(GLP-1) on advanced oxidation protein products (AOPPs)-induced apoptosis of cardiomyocytes. Methods The H9C2 cells were selected in this study and divided into blank control group,RSA control group,and groups treated with indicated concentrations of AOPPs with or without GLP-1,and AOPPs +GLP-1+LY294002 for 24 hours respectively. Cell viability was detected by CCK-8 assay. The ROS level was detected by DCFH-DA fluorescent probe. The cell apoptosis was tested by fluorescent staining and flow cytometry. The expression of p-Akt,p-Bad,Bcl-2,Bax,and active-caspase-3 proteins were evaluated by Western blot. Results GLP-1 attenuated AOPPs-induced cytotoxicity[(0.929±0.083) vs (1.409±0.099),P<0.01],decreased AOPPs-induced ROS[(47.817±0.878)% vs (25.413±2.597)%,P<0.01] and apoptosis[(15.773±3.130)% vs (9.715±0.757)%,P<0.01]. GLP-1 improved AOPPs-induced phosphorylation of Akt and Bad,increased the expression of Bcl-2,and decreased the expression of Bax and the activation of caspase-3. Conclusion GLP-1 protects cardiomyocytes against AOPP-induced apoptosis,predominantly via the PI3K/Akt/Bad pathway.

OBJECTIVETo explore the effect of heat shock protein 90 (HSP90) inhibitor (17-DMAG) and oxaliplatin on the proliferation and invasion of colorectal cancer.

METHODSAfter 17-DMAG, oxaliplatin and half-dose combination of 2 drugs processing colorectal cancer SW480 and HCT116 cell lines, CCK8 assay was applied to detect cell viability. RT-PCR and Western blot were used to detect the expression level of the apoptosis-related molecules. Transwell chemokine axis experiment and Western blot were employed to detect cell invasion ability and the expression level of tumor metastasis-associated protein.

RESULTSThe growth of SW480 and HCT116 cells was inhibited after the administration of 17-DMAG and oxaliplatin(P<0.05) in dose- and time-dependent manner. Processed by 17-DMAG 100 nmol/L, oxaliplatin 50 mg/L and half-dose combination of 2 drugs, transcription level of the apoptosis inhibitory gene (Bcl-2) in SW480 and HCT116 cells was decreased, the level of apoptosis promoting gene (Bax) transcription and protein PARP-1 spliceosome expression was increased, and the above trend was more obvious when using half-dose combination of 2 drugs. Transwell chemokine axis experiments showed the penetrating relative percentage and expression level of MMP9 and integrin β3 decreased, especially for half-dose combination of 2 drugs.

CONCLUSION17-DMAG and oxaliplatin can co-inhibit the proliferation and invasion of colorectal cancer.

Antineoplastic Agents ; Apoptosis ; Benzoquinones ; Cell Proliferation ; Cell Survival ; Colorectal Neoplasms ; HCT116 Cells ; Humans ; Lactams, Macrocyclic ; Neoplasm Invasiveness ; Organoplatinum Compounds