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Cytokine-induced killer (CIK) cells were isolated and proliferation from human peripheral blood and cultured in appropriate growth medium. The biological characteristics of CIK cells were further determined by the characterization of surface markers by flow cytometry. CIK cells inhibited the proliferation of human lung adenocarcinoma NCL-H157 cells. Vascular endothelial growth factor (VEGF) expression was down-regulated in CIK cells co-cultured with NCL-H157 cells by western blotting analysis. Furthermore, in comparison with cells untreated by CIK, the NCL-H157 had a lower proliferation capacity. We proposed that the pharmacological mechanisms of NCL-H157 promoted by CIK can be estimated possibly with different biological significance that can be ascribed to down-regulated VEGF expression in vitro. The results suggest that the VEGF pathway guides developmental inhibiting of NCL-H157, and we speculate that the function of VEGF pathways is to guide NCL-H157 to inhibition by abundant CIK.

Background Adenocarcinoma, the most common form of lung cancer, is one of main human malignant tumors. In this paper, we focus on the effect of antitumor activity of cytokine-induced killer ( CIK) cells on human lung adenocarcinoma cell line A549. Methods CIK cells were obtained by inducing peripheral blood mononuclear cells with recombinant human (rh) interferon-gamma, monoclonal anti- CD3 antibody, rh interleukin (IL)-1alpha, and rhIL-2, which were added into the culture. A549 cell viability of CIK cells was determined using MTS assay. Flow cytometry ( FCM) experiments were performed to detect cell cycle changes. The expression of P27 in A549 cells treated by CIK cells was evaluated by Western blot. Result The percentage of CD3+ CD16+ CD56+ T cells in a representative peripheral blood mononucleated cell sample was 33.7 ± 1.3%. CIK cells, in dose and time dependent manners, inhibited the proliferation of A549. FCM demonstrated that A549 cells were accumulated in G2/M and G0/G1 phases when treated with CIK cells. FCM was used to analyze whether A549 cells treated with CIK cells induced apotosis or necrosis at 10:1 or 20:1. Compared to the control group, P27 was prominently upregulated in the CIK treated group. Conclusion We propose that the pharmacological mechanisms of A549 cells inhibited by CIK cells can be estimated to possibly elicit different biological significance, which, in part, can be ascribed to a different mass transport rate in vitro. [ABSTRACT FROM AUTHOR]

To investigate the mechanism of combination therapy of propofol and sevoflurane on MAP2K3 level and myocardial apoptosis induced by ischemia-reperfusion (IR) in rat. A total of 30 SD rats were randomly separated into 3 groups: normal, IR (ligation of left coronary artery), and IR+ propofol and sevoflurane (IR+P+S). Different methods were used to detect the serum index associated IR injury. TUNEL assay was used to analyze the apoptotic cells of rat heart tissues. qRT-PCR was used to analyze the mRNA levels of cell apoptosis related proteins such as Bcl-2, Bax, and MAP2K3. Western blotting was used to detect the expression of Bcl-2, Bax, MAP2K3, and Caspase-3 of heart tissues. Compared with normal group, serum LDH, cTnI, and CK-MB levels in IR group were significantly increased with time increasing (P<0.05), while that in IR+P+S group were significantly decreased compared with that in IR group (P<0.05). The percentage of apoptotic cells of heart tissue in IR+P+S group was larger than that in IR group (P<0.05). Compared with IR group, mRNA expression of MAP2K3 and Bax were significantly decreased with Bcl-2 was significantly increased in IR+P+S group (P<0.05). Also, expression of MAP2K3, Caspase-3, and Bcl-2 in IR+P+S group were statistically lower while Bax was statistically higher than that in IR group (P<0.05). Our study suggested that combination therapy of propofol and sevoflurane may protect myocardial cells from damage during IR through decreasing MAP2K3 level and reducing cell apoptosis via Bcl-2/Bax pathway.