Inactivated Sendai virus induces apoptosis in cisplatin-resistant human lung adenocarcinoma A549 cells in vitro and in vivo / 中国比较医学杂志

Objective Cisplatin(DDP)is widely used in the chemotherapy of lung cancer. However, cisplatin resistance represents a major obstacle in its effective treatment. Our preliminary work has demonstrated that inactivated Sendai virus(HVJ-E)shows that it induces apoptosis in murine melanoma cells(B16)and obviously inhibites the tumor growth in tumor-bearing BALB/c nude mice. This study aims to investigate whether inactivated HVJ-E has an effect of inducing apoptosis in cisplatin-resistant A549/DDP lung adenocarcinoma cells in vitro and in vivo. Methods HVJ-E and A549/DDP cells were co-cultured in vitro,and the effect of HVJ-E on the apoptosis in A549/DDP cells was detected by flow cytometry. In addition,HVJ-E was injected into the tumor in vivo, and its oncolytic effect was observed by TUNEL assay of tissue sections and measurement of tumor size. Results After co-cultured with HVJ-E for 12 h,24 h and 36 h, the apoptosis rate of A549/DDP cells in late stage detected by flow cytometry was 7.7%, 12.6% and 18.9%,respectively,showing a significant difference between 12 h and 24 h, and between 24 h and 36 h. TUNEL assay showed that there was more apoptosis in tumor cells in vivo in the experimental group than in the control group. Meanwhile, intratumoral injection of HVJ-E induced a significantly smaller tumor volume in the experimental group compared with the control group(P ﹤ 0.05). Conclusions Our findings indicate that inactivated HVJ-E can induce apoptosis in A549/DDP cells both in vitro and in vivo, and intratumoral injection of inactivated Sendai virus significantly reduces the tumor growth in vivo.

Membrane-expressed InsB15-23 H-2Kd dtSCT can reduce morbidity of type 1 diabetes mellitus in NOD mice / 中国免疫学杂志

Objective:To illuminate the influence of InsB15-23 H-2Kd dtSCT to the morbidity of type 1 diabetes mellitus in NOD mice.Methods:An eukaryotic plasmid encoded membrane-expressed InsB15-23 H-2Kd dtSCT was inoculated into 3 weeks old female NOD mice subcutaneously and the blood sugar and morbidity of type 1 diabetes mellitus were monitored once a week.To illuminate the cellular mechanism of immunologic intervention of membrane-expressed InsB15-23 H-2Kd dtSCT to the course of type 1 diabetes mellitus in NOD mice,the mononuclear cell infiltration of islets was detected by tissue slice and the frequency of IGRP206 2-14 specific CTLs in PBMC was analyzed by FACs.Results: As compared with pcDNA3.1 (-) control ( 60%) and untreated NOD mice ( 80%) , mice immunized with InsB15-23 H-2Kd dtSCT exhibited low level of islet infiltration and low morbidity in 30 weeks old ( 9%) .But the frequency of IGRP206-214 specific CTLs in PBMC of 16 and 40 weeks old mice showed no difference.Conclusion:Membrane-expressed InsB15-23 H-2Kd dtSCT can protect NOD mice from type 1 diabetes mellitus in IGRP206-214 independent pattern.