ObjectiveTo investigate the effect of icaritin on the small cell lung cancer cell lines NCI-H446 and its mechanism. MethodsThe NCI-H446 cells at logarithmic growth phase were divided into control and icaritin groups. The cells in the control group were normally treated and cells in the icaritin group were incubated with icaritin (8 μmol/L). Thiazole blue and flow cytometry were used to examine the proliferation and apoptotic changes in the two groups 48 hours after incubation respectively. Gene expression of Janus kinase 2 (JAK2) and signal transducers and activators of transcription 3 (STAT3) were detected by real-time quantitative polymerase chain reaction. The changes of JAK2, STAT3, phospho-JAK2 (p-JAK2), phospho-STAT3 (p-STAT3), Bax and BCL-2 protein were detected by Western blotting. ResultsCompared with the control group, the proliferation rate of NCI-H446 cells in the icaritin group was significantly lower (P<0.05), but the apoptotic rate of NCI-H446 cells in the icaritin group was significantly higher (P<0.05). After the treatment with icaritin, the expression of JAK2 and STAT3 mRNA had no obvious differences. The Western blotting results showed that there was no significant changes in total JAK2, STAT3 protein (P>0.05), but an increasing trend in p-JAK2, p-STAT3 and Bax was observed with the decreasing of BCL-2 (P<0.05). ConclusionIcaritin can inhibit the proliferation and promote the apoptosis of NCI-H446 cells and the effect may be achieved through JAK2/STAT3 signal transduction pathway.
Objective To evaluate the effect of left atrial enlargement on atrial myocardial fibrosis degree and levels of the angiotensinⅡ (AngⅡ)/Rac GTPase activating protein 1 (Rac1)/signal transducersand activators of transcription 3 (STAT3) signaling pathways expressing in patients with persistent atrial fibrillation and rheumatic heart disease (RHD). Methods From March to December 2011, 30 patients with RHD who underwent prosthetic valve replacement in our hospital were enrolled, including 16 males and 14 females, aged 42-70 (56.9±6.8) years. Twenty RHD patients with persistent atrial fibrillation as a research group and ten RHD patients with sinus rhythm as a control group (group A) underwent transthoracic echocardiography and right atrial appendage (RAA) tissue samples were obtained from these patients during mitral/aortic valve replacement operation. The research group according to left atrial diameter (LAD) was divided into two groups, ten patients in each group: a group B with LAD of 50–65 mm and a group C with LAD of LAD>65 mm. For each sample, histological examination was performed by hematoxylin-eosin and Masson’s trichrome staining. Light-microscopic pictures of atrial tissues samples were stained and tissue fibrosis degree in each group was analyzed. AngⅡ concentration was measured by enzyme linked immunosorbent assay. Rac1 and STAT3 were measured by western blotting. Results LAD was significantly greater in AF patients with RHD than in the control group. Hematoxylin-eosin staining demonstrated highly organized arrangement of atrial muscles in the control group and significant derangement in both group B and group C with reduced cell density and increased cell size. Moreover, Masson’s trichrome staining showed that atrial myocytes were surrounded by large trunks of collagen fibers in both group B and group C, but not in the group A. There was a positive correlation between atrial tissue fibrosis and LAD. AngⅡ content was positively correlated with LAD. Similarly, Rac1 and STAT3 protein levels were found considerably higher in the group C and group B than in the group A with excellent correlation to LAD. Conclusion In patients with RHD complicated with persistent atrial fibrillation, the degree of atrial fibrosis and the expression level of AngⅡ/Rac1/STAT3 signaling pathways significantly increase with the left atrialenlargement.