The aim of this study was to investigate the effects of β-catenin on the tumorigenicity of K562 cells in vivo. The β-catenin expression in K562 cells was down-regulated through sequence-specific siRNA, and the treated K562 cells were implanted into BALB/c nude mouse subcutaneously. And the tumor-forming rate and tumor-forming curve (interference group) were observed. Experiments were divided into 3 group: interference group (implanted K562 cells transfected with β-catenin interfering plasmid DNA), control group (implanted K562 cells transfected with unrelated sequence plasmid DNA) and untreated group (implanted K562 cells transfected without plasmid DNA). The results indicated that the tumor-forming rates of untreated group (n = 9), control group (n = 8) and interference group (n = 9) were 100%, 87.5% and 0% respectively. The tumor-forming rate of interference group was significantly lower than those of the other 2 groups (p < 0.001). Comparison of the tumor-forming curve between 3 groups, showed that in first 2 groups existed tumor-forming and their final tumor volumes were almost the same, but the tumor growth of untreated group was faster than that in control group; while in the interference group there was not tumor-forming. It is concluded that the β-catenin expression level in K562 cells is down-regulated through the interference of sequence-specific siRNA, thus affecting their tumor-forming potential in vivo.
Animals ; Apoptosis ; Cell Proliferation ; Humans ; K562 Cells ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; RNA, Small Interfering ; genetics ; beta Catenin ; metabolism

BACKGROUNDNitric oxide (NO) is an important mediator in the pathophysiology of many vascular diseases. However, the definite role of NO in human abdominal aortic aneurysm (AAA) formation is unclear. The aim of this study was to investigate production of NO and expression of inducible nitric oxide synthase (iNOS), and their possible role in AAA.

METHODSA total of 28 patients with AAA, 10 healthy controls, and 8 patients with arterial occlusive disease were enrolled into this study. Standard colorimetric assay was used to examine NO concentration in plasma from patients with AAA and normal controls, and in cultured smooth muscle cells (SMCs). Expression of iNOS in aortas and cultured SMCs were detected by immunochemistry. The correlation of iNOS expression with age of the patient, size of aneurysm, and degree of inflammation was also investigated by Cochran-Mantel-Haenszel chi2 test and Kendall' Tau correlation.

RESULTSExpression of iNOS increased significantly in the wall of aneurism in the patients with AAA compared to the healthy controls (P < 0.05) and the patients with occlusive arteries (P < 0.05). iNOS protein and media NOx (nitrite + nitrate) also increased in cultured SMCs from human AAA (n = 4, P < 0.05), while plasma NOx decreased in patients with AAA (n = 25) compared to the healthy controls (n = 20). There was a positive correlation between iNOS protein and degree of inflammation in aneurismal wall (Kendall coefficient = 0.5032, P = 0.0029).

CONCLUSIONSSMCs and inflammatory cells were main cellular sources of increased iNOS in AAA, and NO may play a part in pathogenesis in AAA through inflammation.

Adult ; Aged ; Aortic Aneurysm, Abdominal ; etiology ; Apoptosis ; Female ; Humans ; Male ; Middle Aged ; Muscle, Smooth, Vascular ; pathology ; Nitric Oxide ; physiology ; Nitric Oxide Synthase Type II ; analysis ; physiology

Enterovirus 71 (EV71) infection is more likely to cause hand, foot and mouth disease (HFMD) in children, which can lead to neurogenic complications and higher mortality. As a commonly used clinical medicine, Reduning injection (RDN) helps to shorten the symptoms of patients with HFMD and facilitate the early recovery of children. However, the regulatory mechanism of RDN on the HFMD immune system disorder caused by EV71 remains to be discussed. This study collected detailed treatment data of 56 children with HFMD who entered the affiliated Children's Hospital of Nanjing Medical University during 2019. Retrospective analysis of clinical data showed that the symptoms of the RDN treatment group were improved compared with the untreated group. To explore its mechanism, the relevant detection indicators were detected by flow cytometry, enzyme-linked immunosorbent assay and real-time quantitative PCR. It was found that the number and function of innate immune (ILCs) and adaptive immunity (Th1, Th2 and secreted cytokines) were reduced, suggesting that RDN plays a role by regulating cellular immunity. The in vitro differentiation inhibition test further confirmed that RDN affected Th1 differentiation by inhibiting the expression of transcription factors on the basis of Th1 cell differentiation in vitro.