RESUMEN
[Purpose] To assess the effects of Tai Chi on the renal and cardiac functions of patients with chronic kidney disease (CKD) and cardiovascular disease (CVD). [Subjects and Methods] Twenty-one patients with CKD and CVD were randomly divided into control and exercise groups. The exercise group performed Tai Chi training for 30 minutes three to five times a week for 12 weeks, while the control group did not. All patients' renal and cardiac functions and blood lipid parameters were measured at baseline and after 12 weeks. [Results] The 12 weeks Tai Chi intervention improved the estimated glomerular filtration rate (eGFR), left ventricular ejection fraction (LVEF), and the high density lipoprotein (HDL) level, and decreased the serum creatintine (Scr) level, heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and the total cholesterol (CH), triglyceride (TG) and low density lipoprotein (LDL) levels. The change in eGFR correlated negatively with the changes in CH, TG and LDL, and positively with the change in HDL. In addition, the change in SBP correlated positively with the changes in CH, TG and LDL, and negatively with the change in HDL. [Conclusion] Tai Chi training might improve the renal and cardiac functions of CKD and CVD patients via improved regulation of lipid metabolism.
RESUMEN
OBJECTIVE: To explore the roles of NF-κB in factor VIIa-induced proliferation and migration of a colon cancer cell line (SW620) in vitro and its possible mechanism. METHODS: The expression levels of NF-κB (p65), inhibitory protein of NF-κB (IκB-α), caspase-7, interleukin 8 (IL-8) and tissue factor (TF) in SW620 cells treated with factor VIIa, PDTC (an inhibitor of NF-κB) and other factors were measured by Western-blotting and real-time PCR. Proliferation and migration of the cells were analyzed by flow cytometry and Transwell assay, respectively. RESULTS: Factor VIIa down-regulated the IκB-α level in SW620 cells and increased the intranuclear level of NF-κB. Those effects of factor VIIa were blocked by anti-TF or anti-PAR2 antibodies. The effects of factor VIIa on proliferation and migration of SW620 cells, expression of IL-8, TF as well as caspase-7, were interfered by PDTC (the inhibitor of NF-κB). CONCLUSIONS: TF/VIIa complex activates NF-κB pathway via PAR2, thereby up-regulates IL-8 and down-regulates caspase-7 expression in SW620 cells, finally promotes proliferation and migration of colon cancer cells. In addition, TF/VIIa/PAR2/NF-κB pathway also upregulates TF expression, thus to create a positive feedback loop of TF/VIIa/PAR2/NF-κB/TF.
Asunto(s)
Movimiento Celular/efectos de los fármacos , Proliferación Celular/efectos de los fármacos , Neoplasias del Colon/patología , Factor VIIa/farmacología , Proteínas I-kappa B/metabolismo , Factor de Transcripción ReIA/metabolismo , Antineoplásicos/farmacología , Caspasa 7/genética , Caspasa 7/metabolismo , Línea Celular Tumoral , Neoplasias del Colon/metabolismo , Humanos , Interleucina-8/genética , Interleucina-8/metabolismo , Inhibidor NF-kappaB alfa , Prolina/análogos & derivados , Prolina/farmacología , ARN Mensajero/metabolismo , Receptor PAR-2/metabolismo , Tiocarbamatos/farmacología , Tromboplastina/genética , Tromboplastina/metabolismo , Factor de Transcripción ReIA/antagonistas & inhibidoresRESUMEN
AIM: To investigate whether tumor necrosis factor receptor-associated factor 6 (TRAF6) is involved in anti-ß2GPI/ß2GPI-induced tissue factor (TF) expression on THP-1 cells. METHODS: The total RNA was extracted and the protein lysates were collected from THP-1 cells stimulated with anti-ß2GPI/ß2GPI complex. And then the TF expression on THP-1 cells was detected by real-time quatitative PCR (RT-qPCR) and TF activity kit. TRAF6 mRNA and its protein expression were investigated by RT-qPCR and Western blotting, respectively. The proteasome inhibitor, MG-132, was used for inhibitory assays, in order to demonstrate the effect of anti-ß2GPI/ß2GPI complex on THP-1 cells. RESULTS: The TF expression (both mRNA and activity) on THP-1 cells was significantly up-regulated with the treatment of anti-ß2GPI/ß2GPI complex (100 mg/L), compared with untreated cells(P<0.05). The TRAF6 mRNA and protein levels in THP-1 cells were also significantly increased with the treatment of anti-ß2GPI/ß2GPI complex. The expression of TRAF6 was shown in a time-dependent manner, with the maximal level at 15 minutes (mRNA) and 30 minutes (protein) respectively. All the stimulating effects of anti-ß2GPI/ß2GPI complex (100 mg/L) on THP-1 cells were inhibited by MG-132 (5 µmol/L). CONCLUSION: TRAF6 is up-regulated and contributes to TF expression on THP-1 cells induced with anti-ß2GPI/ß2GPI complex.