Objective To investigate the clinical values of continuous hemoperfusion on the level of inter-leukin-18(IL-18)and prognosis in patients with acute paraquat poisoning(APP). Methods A total of 112 pa-tients with APP treated in our hospital from Jun 2013 to Jul 2017 were divided into two groups:control group(56 cases,routine drug and single hemoperfusion)and therapy group(56 cases,treated by continuous hemoperfusion based on control group).All APP patients were treated with continuous veno venous hemofiltration(CVVH)at 24 hours after treatment.Within admission 24 hours,3 days and 7 days after treatment,IL-18,lactic acid(Lac),ar-terial oxygen partial pressure(PaO2),alanine aminotransferase(ALT),creatinine(Cr)and creatine kinase(CK-MB)of patients were detected,28-day survival was recorded.Pearson correlation test was used to analyze the corre-lation between IL-18 in patients with APP and the survival rate. Results In admission,there were no differences in the levels of IL-18,Lac,PaO2,ALT,Cr and CK-MB between the two groups(P>0.05).At 3 days after treat-ment,the levels of IL-18,Lac,ALT,Cr and CK-MB were higher than those before treatment,and the therapy group was lower than the control group,while PaO2was lower than those before treatment,and the therapy group was higher than the control group(P<0.05);At 7 days after treatment,the two groups both had lower levels of IL-18,Lac,ALT,Cr and CK-MB than those after 3 days treatment,and the therapy group was lower than the con-trol group,while PaO2was lower than those after 3 days treatment,and the therapy group was higher than the con-trol group(P<0.05);There were 39 deaths in the therapy group and 49 deaths in the control group,the therapy group had a lower 28-day mortality rate than control group,the difference was statistically significant(69.64% vs 87.50%,χ2=5.303,P=0.021). The level of serum IL-18 in patients with APP was negatively correlated with the survival rate(r =-0.209,P = 0.027).Conclusions Therapeutic effect of continuous hemoperfusion in APP pa-tients is superior to single hemoperfusion. It could decrease the levels of IL-18,Lac,ALT,Cr and CK-MB,im-prove PaO2 and reduce the mortality rate of patients.The clinical curative effect is distinct.

OBJECTIVE: To investigate the effect of down-regulation of pannexin 2 (Panx-2) channels on cisplatin-induced apoptosis in I-10 cells. METHODS: The expression of Panx-2 protein in testicular cancer cells was detected with Western blotting. The testicular cancer cell line I-10 was transfected with two short hairpin RNA (shRNA1 and shRNA2) Lipofectamine, the empty vector (NC group) or Lipofectamine2000 (blank control group), and the changes in the expression of Panx-2 was detected with Western blotting. The effects of transfection with a Panx-2 inhibitor on surviving fraction of the cells treated with cisplatin (16 μmol/L) for 24 h, 48 h and 72 h was assessed with MTT assay, and the clonogenic capacity of the cells was evaluated with colony-forming assay. At 8 h after incubation with 16 μmol/L cisplatin, AnnexinV/PI double staining was used to detect the early apoptosis of the cells. After 24 h of treatment with 16 μmol/L cisplatin, the cells were examined for expressions of caspase-3, Bcl-2 and Bax using Western blotting. RESULTS: The expression of Panx-2 was significantly increased in cisplatin-resistant I-10/DDP ( < 0.001) cells and Tcam-2/DDP ( < 0.01) cells as compared with I-10 cells and Tcam-2 cells. Transfection of I-10 cells with shRNA1 and shRNA2 resulted in significantly decreased Panx-2 expression ( < 0.05) and significantly reduced cell surviving fraction ( < 0.001). In the presence of cisplatin, the cells in NC group showed a higher clonogenic efficiency than those in shRNA1 and shRNA2 groups ( < 0.001). The early-stage apoptosis rate of the cells in shRNA1 and shRNA2 groups were significantly higher than that in NC group ( < 0.01). Panx-2 knockdown in I-10 cells significantly increased caspase-3 and Bax expressions ( < 0.05) and significantly decreased the expression of Bcl-2 ( < 0.01). CONCLUSIONS Down-regulation of Panx-2 channel enhances cisplatin-induced apoptosis in cultured testicular cancer cells.
Antineoplastic Agents ; Apoptosis ; Cell Line, Tumor ; Cell Proliferation ; Cisplatin ; Connexins ; Down-Regulation ; Drug Resistance, Neoplasm ; Humans ; Male ; Testicular Neoplasms