J. Yu’s scientific contributions

Objective: To investigate the role of programmed cell death 5 (PDCD5) protein in apoptosis of prostate cancer PC-3M cells induced by mifepristone (MIF) and elucidate the possible mechanism. Methods: The viability of PC-3M prostate cancer cells after incubation with MIF at 5, 10, 20, 50, and 100 μmol/L for 24-96 h were measured by MTT assay. The optimal incubation time and drug concentration were determined. PCI-neo-PDCD5 was transfected into PC-3M cells via liposome mediation, and the PDCD5 protein expression was detected by using immunofluorescence method. After the transfected PC-3M cells were treated with 20 μmol/L MIF for 24 and 48 h, the apoptosis was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and acrine range (AO)/enthidium bromide (EB) staining, respectively. Western blotting was used to examine the expression of apoptosis-related protein caspase 3. Results: The absorbance values of the PC-3M prostate cancer cells treated with 5 and 10 μmol/L of MIF were similar to that of controls (P < 0.05), while those of the cells treated with 20, 50 and 100 μmol/L of MIF were significantly decreased compared with that of controls (P < 0.01). It indicated that MIF markedly inhibited the proliferation of prostate cancer PC-3M cells in a dose-and time-dependent manner. PCI-neo-PDCD5 was successfully transfected and transiently expressed in PC-3M cells. Compared with the control and single MIF treatment group, the apoptosis ratio was significantly increased in PDCD5 transfected and MIF-treated group (P < 0.01). Western blotting showed that the expression of caspase 3 protein was significantly increased in PC-3M cells after transfection with PCI-neo-PDCD5 and treatment with 20 μmol/L MIF for 48 h (P < 0.01). Conclusion: Exogenous PDCD5 protein had synergistic effects with MIF in inducing apoptosis of PC-3M prostate cancer cells. It suggested that PDCD5 has the potential to become an adjuvent drug for prostate cancer therapy in clinic.

OBJECTIVE: To study the protective effect and mechanism of quercetin(Que) on doxorubicin(Dox)-induced damage to cardiomyocytes in neonate rats in terms of Fas/FasL and oxidative stress. METHODS: Cultured neonatal rat cardiomyocytes were randomly divided into 5 groups: normal control group, Dox 1.72 μmol · L-1 group, Dox + Que 25, 50 and 100 μmol · L -1 groups. The cells in Dox + Que groups were pretreated with Que for 3 h and then co-incubated with Dox for 24 h. To observe the cell growth condition by inverted microscope, the activity of glutathion peroxidase (GSH-Px) and superoxide dismutase (SOD) was detected by chromatometry; the mRNA and protein expression of Fas and FasL was detected by RT-PCR and Western blotting, respectively. RESULTS: Compared with normal control group, the activity of GSH-Px and SOD in Dox group decreased; and the mRNA and protein expression of Fas and FasL was up-regulated. Que 25 ,50 and 100 μmol · L -1 could act as an antagonist of changes induced by Dox : GSH-Px, (76 ± 3) , (73 ± 4), (71 ± 3) vs (69 ± 3) kU · L-1 ; SOD, (31 ± 2) , (29 ± 2) , (29 ± 2) vs (26 ± 2) kU · L-1 ; Fas mRNA:0.61 ± 0. 11, 1.04 ± 0. 12, 1.29 ± 0. 11 vs 1.61 ± 0. 16; FasL mRNA:0. 81 ± 0.07, 1.24 ± 0.10, 1.57 ± 0.09 vs 1.79 ± 0.11; Fas protein: 1.08 ± 0.12, 1.54 ± 0.10, 1.89 ± 0.11 vs 2.15 ± 0.15; FasL protein : 1.51 ± 0.08, 1.70 ± 0.12, 2.20 ± 0.09 vs 2.41 ± 0.26. CONCLUSION: Que may significantly inhibit the apoptosis induced by Dox in the cultured myocardial cells. The potential mechanism is that Que can down-regulate Fas and FasL protein expression.

Aim: To observe the protective effect of quercetin on rat cardiomyocyte apoptosis induced by adriamycin and explore its possible mechanism. Methods: Cultured neonatal rat cardiomyocytes were randomly divided into six groups: normal control group, adriamycin group, quercetin control group, adriamycin + quercetin (25,50,100 μmol·L-1) groups. The activity of LDH was detected by chromatometry, the cardiomyocyte viability was measured by MTT, the ultrastructure of cardiomyocyte was observed by electron microscope, the expression of protein Bcl-2 and Bax was analyzed by immunocytochemical, and the mRNA and protein of caspase-3 were detected by RT-PCR and Western blot respectively. Results: Compared with the control group, the activity of LDH was increased but the viability of cardiomyocyte was decreased; the expression of Bax and caspase-3 was up-regulated while Bcl-2 was down-regulated in ADR group. Compared with ADR group, the above changes were lightened in adriamycin + quercetin groups. But the quercetin control group, in which cultured myocardial cells only exposed to quercetin without ADR, had no obvious changes. Conclusions: Quercetin significantly inhibits the apoptosis induced by ADR in the cultured myocardial cells. Its mechanism is involved in the apoptosis-related pathways, including caspase-3, Bax and Bcl-2.