Contrast-enhanced transrectal ultrasonography in guiding prostate biopsy for diagnosis of prostate cancer / 中国介入影像与治疗学

Objective: To explore the value of contrast-enhanced transrectal ultrasonography (CETRUS) in guiding prostate biopsy for diagnosis of prostate cancer (PCa). Methods Transrectal ultrasound (TRUS), CETRUS and transrectal prostate biopsy were performed in 79 patients with suspected PCa. The diagnosed efficiency of TRUS, CETRUS and TRUS combined CETRUS were compared and taken pathology results as diagnostic criteria. Results Among 79 patients, PCa was pathologically diagnosed in 36 cases, while benign prostatic hyperplasia was diagnosed in 43 cases. Pathology results proved PCa in 30 patients among 35 patients with abnormal CETRUS, and the sensitivity, specificity and accuracy of CETRUS for diagnosing PCa was 83.33% (30/36), 88.37% (38/43) and 86.08% (68/79), respectively. Pathology results proved PCa in 24 patients among 39 patients with abnormal TRUS, and the sensitivity, specificity and accuracy of TRUS for diagnosing PCa was 66.67% (24/36), 65.12% (28/43) and 65.82% (52/79), respectively. Thirty cases of PCa were diagnosed with TRUS combined CETRUS, and the sensitivity, specificity and accuracy was 83.33% (30/36), 72.09% (31/43) and 77.22% (61/79), respectively. ROC curve analysis showed that the AUC of TRUS, CETRUS and TRUS combined CETRUS was 0.740, 0.859 and 0.777,respectvely. The diagnostic efficiency of CETRUS was higher than that of TRUS (Z=2.371, P=0.018) and TRUS combined CETRUS (Z=2.858, P=0.004). Conclusion: The diagnostic efficiency of CETRUS is high for guiding transrectal prostate biopsy to diagnose PCa.

The inhibitory effect of OSTP-DDP on the growth of ovarian cancer A2780 cells / 中国药理学通报

Aim To study the growth inhibitory effect of the conjugate ( ovarian cancer specific targeting peptide and cisplatin, OSTP-DDP ) that targeting ovarian cancer cells A2780. Methods Using chemical method to syn-thesize OSTP-DDP, ovarian cancer cells A2780 were cul-tured in vitro, using CCK-8 method ( Cell Counting Kit-8) to detect the growth inhibitory effect of ovarian cancer A2780 cells, which were disposed by OSTP-DDP and DDP. Annexin V-FITC was used to detect the cycle and apoptosis effect of ovarian cancer A2780 cells which were disposed by OSTP-DDP and DDP. Results According to the mass spectrometry and the high performance liquid chromatography ( HPLC ) analysis, OSTP-DDP was proved to synthesize successfully. CCK-8 assay showed that both OSTP-DDP and DDP could play the growth in-hibitory effect and showed a concentration-dependent manner when cells were treated in different concentrations (10,20,40,80,160,320μmol·L-1 ) respectively after 24 h, 48 h, 72 h. And the effect of OSTP-DDP was stronger than DDP (P<0. 05), indicated OSTP-DDP had targeted cytostatic effect. The result of the flow cytometry showed that cell cycle was mostly arrested in G1 phase after 72h treated by OSTP-DDP and DDP, the inhibitory effect of OSTP-DDP was stronger than DDP (P<0. 05). The apop-tosis effect of OSTP-DDP was stronger than DDP ( P <0. 01),suggested that OSTP-DDP had a stronger targeting apoptosis-inducing effect. Conclusion OSTP-DDP has the targeting growth inhibitory effect on the ovarian cancer cell A2780, OSTP as a chemotherapeutic drug targeting vector has a great prospect to treat ovarian cancer.

The study of miR-216a induces cell apoptosis by targeting PKCαin gastric cancer / 重庆医学

Objective To confirm whether miR-216a suppresses cell proliferation and induces cell apoptosis by targeting PKCα, thus to reveal molecular mechanism that miR-216a functions as a tumor suppressor in gastric cancer .Methods PKCα3′untranslat-ed region(UTR)-luciferase vector was constructed and dual-luciferase reporter gene assay was employed to examine the effect of miR-216a on luciferase activity .MGC-803 cells were transfected with miR-216a mimics ,and next Western blotting was performed to detect the expression of PKCαprotein .The effects of PKCαdownregulation on cell proliferation and apoptosis were observed after PKCαsiRNA were transfected into MGC-803 cells .MGC-803 cell proliferation assays were performed when cotransfected with miR-216a mimics .Results The result demonstrated miR-216a could bind to the 3′UTR of PKCαand inhibited the luciferase activi-ty ,cut the 41% .PKCαprotein expressions were significantly down-regulated when miR-216a was overexpressed in MGC-803 .siR-NA-mediated downregulation of PKCα could suppress the potentials of cell proliferation and induce apoptosis .Conclusion miR-216a suppresses cell proliferation and induces apoptosis by targeting PKCαmRNA 3′UTR in gastric cancer .

Role of reactive oxygen species in the apoptosis of human hepatocellular carcinoma HepG_2 cells induced by PIG11 protein overexpression / 肿瘤

Objective:To investigate the role of reactive oxygen species (ROS) in the apoptosis of human hepatocellular carcinoma HepG_2 cells induced by PIG11 protein overexpression. Methods:The fluorescent probe 2', 7'-dichlorofluorescin diacetate (DCFH-DA) was used to label the intracellular ROS in pLXSN-PIG11-HepG_2 cells,pLXSN-HepG_2 cells and HepG_2 cells.The intracellular fluorescence intensity was detected by using the flow cytometry (FCM). The apoptotic ratio of HepG_2 was determined by FCM after elimination of intracellular ROS with 10 mmol/L N-acetylcystine (NAC). Results:The intracellular content of ROS in pLXSN-PIG11-HepG_2 cells was significantly higher than that in pLXSN-HepG_2 cells[(15.60±0.92) vs (4.90±0.70), P<0.01)]. The apoptotic ratio of pLXSN-PIG11-HepG_2 cells was significantly decreased by pretreatment with 10 mmol/L NAC (P<0.01). Conclusion:The apoptosis-inducing effect of PIG11 over-expression is related with elevation of intracellular ROS levels.

Role of intracellular Ca~(2+) in diallyl trisulfide induction of apoposis in gastric cancer cells / 中国药理学通报

Aim To investigate whether DATS induce MGC803 cell apoptosis and the relationship betweenapoptosis and Ca~(2+) disruption. Methods MGC-803 cell growth inhibition was measured by MTT assay. Tunnel and flow cytometry methods were used to determine the induction of apoptosis and Ca2+ homeostasis disruption. Result MTT assay showed that the inhibitory rates on MGC-803 cell growth of different concentrations of DATS 4,8,12,16 and 24 mg?L-1 were 0.231?0.037,0.305?0.036,0.455?0.029,0.607?0.058,0.751?0.019 respectively. Flow cytometry analysis showed that treating MGC803 cell with DATS significantly increased the percentage of apoptosis cells and intracellular Ca2+. Treatment of cells with 1,2-bis(2-aminophenoxye-thane)-N,N,N-tetraacetic acid tetrakis acetoxymethyl ester (BAPTA-AM), cellular Ca2+ chelator, resulted in abolishment of the elevation of intracellular Ca~(2+) and blockage of DATS induced apoptotic of MGC-803. Conclusoin DATS could induce apoptosis of MGC-803 cells through the mechanism of Ca~(2+) homeostasis disruption.

Effect of TRF1,TRF2 and telomeric stability on As_2O_3 induced MGC803 cell apoptosis / 中国药理学通报

Aim To study the effect of As_2O_3(arsenic trioxide) on the expressions of telomeric repeat binding factor1,2 and telomeric stability of human gastric cancer MGC803 cells, and explore the mechanism of cell apoptosis. Method MGC803 cell growth inhibition was measured with MTT assay. Apoptosis was analyzed with flow cytometry. Influence on chromosome distal end was analyzed with chromosome end-end fusion analysis. Expressions of TRF1 and TRF2 were determined with Western blot analysis. Results MTT assay showed that As_2O_3 clearly inhibited the growth of MGC803 cells, depending on time and dosage. The apoptosis rates were significantly higher than those of the control group in a concentration and time-dependent manner. These changes were not found in the control group. After disposal with 5 ?mol?L -1 As_2O_3, chromosome fusion rate was obviously increased in 48 h. After 48 h of disposal with 5 ?mol?L -1 As_2O_3, the TRF1 of MGC803 cells was up-regulated while TRF2 was down-regulated. Conclusion As_2O_3 induced chromosome fusion and MGC803 cells apoptosis through up-regulating expressin of TRF1 and down-regulating expressin of TRF2.

Construction of a subtracted cDNA library of differentially expressed genes in human gastric carcinoma induced by diallyl disulfide / 中国药理学通报

Aim To construct a subtracted cDNA library o f differentially expressed genes in human gastric carcinoma induced by diallyl dis ulfide(DADS). Methods Differentially expressed cDNA species induc ed by DADS in MGC 803 human gastric carcinoma cell line was determined by using suppression subtractive hybridization (SSH). Then these cDNA species were direct ly inserted into T/A cloning vector to set up the subtractive library. Amplification of th e library was carried out with transformation of E.coli by high voltage electrop erforation. One hundred positive bacteria clones were randomly picked and identi fied using PCR method. Results The amplified library contained more than 1,000 positive bacteria clones. Random analysis of 100 clones with PCR m ethod showed that all clones contained 100～600 bp inserts.Conclusions A subtracted cDNA library of differentially expressed genes in MGC 803 hum an gastric carcinoma cell line induced by DADS is constructed successfully with SSH and T/A cloning techniques. The library is efficient and lays solid foundati on for screening and cloning new and specific tumor correlative genes of human g astric carcinoma, and provides a new idea for further exploring the mechanism of DADS effects on carcinoma cells.

Apoptosis, myocardial fibrosis and angiotensin II in the left ventricle of hypertensive rats treated with fosinopril or losartan / 中华医学杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the different effects of an angiotensin II type 1 (AT(1)) receptor antagonist, losartan, and an angiotensin converting enzyme (ACE) inhibitor, fosinopril, on cardiomyocyte apoptosis, myocardial fibrosis, and angiotensin II (Ang II) in the left ventricle of spontaneously hypertensive rats (SHRs).</p><p><b>METHODS</b>SHRs of 16-week-old were randomly divided into 3 groups: SHR-L (treated with losartan, 30 mg.kg(-1) x d(-1)), SHR-F (treated with fosinopril, 10 mg x kg(-1) x d(-1)), and SHR-C (treated with placebo). Each group consisted of 10 rats. Five rats, randomly selected from each group, were killed at the 8th and 16th week after treatment. Cardiomyocyte apoptosis, collagen volume fraction (CVF), perivascular collagen area (PVCA) and Ang II concentrations of plasma and myocardium were examined.</p><p><b>RESULTS</b>Compared with the controls at the 8th and 16th week, systolic blood pressures were similarly decreased in both treatment groups. Left ventricular weight and left ventricular mass indexes were significantly lower in both treatment groups. However, the latter parameter at the 16th week was reduced to a less extent in the fosinopril group than that in the losartan group. Compared with the controls, cardiomycyte apoptotic index was significantly reduced at the 8th week only in the fosinopril group, and at the 16th week in both treatment groups. The index of the fosinopril group was lower than that of the losartan group at the latter endpoint examined. Compared with the controls, the left ventricular collagen volume fraction and perivascular collagen area at the 8th and 16th weeks were significantly reduced in the SHRs treated with either fosinopril or losartan. However, the collagen volume fraction at the latter endpoint in the fosinopril group was lower than that in the losartan group. Compared with the controls at endpoints, plasma and myocardium Ang II levels were significantly increased in the losartan group. However, plasma Ang II concentrations were not altered, and myocardium Ang II concentrations at the 8th and 16th weeks were significantly reduced in the fosinopril group.</p><p><b>CONCLUSIONS</b>Both losartan and fosinopril could effectively inhibit cardiomyocyte apoptosis and myocardial fibrosis and reverse heart hypertrophy. Fosinopril may be more effective in these cardioprotective effects, suggesting that the effects of both drugs are related to the inhibition of myocardium renin-angiotension-aldsterone system.</p>

Effects of Lorsartan, Fosinopril on myocardial fibrosis, angiotensin Ⅱ and cardiac remolding in hypertensive rats / 中南大学学报(医学版)

Objective: To investigate effects of lorsartan, fosinopril on myocardial fibrosis, angiotensin Ⅱ and cardiac remolding in the spontaneously hypertensive rats (SHR). Methods: 16-week-old SHRs were divided randomly into 3 groups: SHR-L (treated with lorsartan), SHR-F (treated with fosinopril) and SHR-C (untreated), each group consisting of 10 rats. After 8 weeks' and 16 weeks' therapeutic period, collagen volume fraction (CVF), perivascular circuferential area (PVCA), plasma and myocardium angiotensin Ⅱ concentrations were examined by pathological examination with computed processing and radioimmunoassay respectively. Results: (1) Compared with SHR-C after 8 weeks' and 16 weeks' therapeutic period, the systolic blood pressure (SBP) was decreased similarly in both treatment groups. Heart and left ventricular weights, heart weight and eft ventricular mass indexes were lower significantly in both treatment groups than in SHR-C. Left ventricular mass index was reduced to a lower extent in SHR-F group than in SHR-L group after 16 weeks. (2) Compared with SHR-C, CVF, PVCA after 8 weeks and 16 weeks were reduced significantly in SHR-F and SHR-L. Meanwhile, CVF after 16 weeks in SHR-F than in SHR-L. (3) Compared with SHR-C after both therapeutic periods, plasma and myocardium angiotensin Ⅱ concentrations were increased Significantly in SHR-L, but plasma angiotensin Ⅱ concentrations were not altered significantly in SHR-F. However, myocardium angiotensin Ⅱ concentrations were reduced significantly in SHR-F after 8 weeks and 16 weeks in SHR-F. Conclusion: Lorsartan, fosinopril inhibit myocardial fibrosis and reverse heart hypertrophy. Fosinopril may be more effective in these above effects than Lorsartan. The mechanism of the both drug's cardioprotective effects was related to inhibition of myocardium rennin-angiotension-aldsteron system.

Effect of growth inhibition of diallyl trisulfide on gastric cancer MGC-803 cell line in vitro / 中国药理学通报

AIM To study the effects of growth inhibition of different concentrations of diallyl trisulfide(DATS) on gastric cancer MGC 803 cell line in vitro. METHODS The influence of different concentrations of DATS were examined by MTT assay, clonal formation rates and cell growth curve. RESULTS Suppression and decrease of MGC 803 cell proliferation was found after treatment by DATS in vitro. The inhibitory rates on MGC 803 cell growth of different concentration of DATS,4, 8, 12, 16 and 24 mg?L -1 , were 26%,46%,65%,76% and 89% respectively, and its half inhibitory concentration (IC 50 ) was 8 2 mg?L -1 . The clonal formation rates and clonal formation relative counts of 8, 12, 16 and 24 mg?L -1 were 32 4% and 58 7%,24 8% and 42 5%,19 0% and 33 5%?8 8% and 15 1% respectively.There was significant correlation between dose and effect in all, and the cell growth culve became lower and flatter when concentration of DATS increase gradually. CONCLUSION The effect of growth inhibition of DATS for gastric cancer MGC 803 cell in vitro is remarkable.