【摘要】 目的 观察替米沙坦对高血压伴阵发性心房颤动患者房颤复发及对左心房内径(LAD)、血清C反应蛋白(HsCRP) 的影响。 方法 2007年6月-2008年12月阵发性房颤患者42例，随机分为替米沙坦组和常规治疗组各21例，分别于治疗前、治疗后12个月测定LAD、HsCRP水平，并随访治疗后12个月时房颤复发次数。 结果 替米沙坦组房颤复发次数及LAD、HsCRP水平均低于常规治疗组，两组比较，有统计学意义(Plt;0.05)。 结论 替米沙坦能抑制高血压伴阵发性房颤患者的左房重构，降低HsCRP水平，减少房颤复发。【Abstract】 Objective To explore the effects of Telmisartan on recurrence of paroxysmal atrial fibrillation (PAF), left atrial direction (LAD) and serum levels of high sensitivity C reaction protein (HsCRP) in patients with hypertension combined with paroxysm atrial fibrillation. Methods A total of 42 PAF patients from June 2007 to December 2008 were randomly divided into Telmisartan group and routine treatment group. Before the treatment and 12 months after the treatment, LAD and HsCRP were detected,and the recurrence times of atrial fibrillation were counted 12 months after the treatment. Results The recurrence times of atrial fibrillation, and the levels of LAD and HsCRP were significant lower in Telmisartan group than that in the routine treatment group (Plt;0.05). Conclusion Telmisartan can reduce the recurrence of PAF and the levels of LAD and HsCRP.
目的:研究替米沙坦对合并高血压的阵发性房颤患者转复为窦性心律后复发的影响。方法: 选择84例合并高血压的阵发性房颤患者,随机分成观察组及对照组,观察组降压药使用替米沙坦,对照组使用氨氯地平,两组均使用胺碘酮复律,随访2年,观察两组患者的疗效及超声心动图(左房内径)变化。结果:观察组治疗合并高血压的阵发性房颤复发率显著低于对照组。结论:替米沙坦联合抗心律失常药物,能有效防止房颤复发,维持窦性心律。
ObjectiveTo investigate the effects of telmisartan on the proliferation, migration and apoptosis of non-small cell lung cancer A549 and the mechanism of regulating Wnt signaling pathway.MethodsNon-small cell lung cancer cell line A549 was cultured in vitro. Cell counting kit-8 (CCK-8) assay was used to detect the effect of telmisartan at different concentrations on the proliferative activity of A549 cells. The survival fraction of A549 treated with different concentrations of telmisartan was determined by colony-formation assay. The effect of telmisartan at different concentrations on the migration ability of A549 cells was examined in the wounding healing assay. Hoechst staining was used to detect the effects of telmisartan at different concentrations on the apoptosis of A549. Western bloting was used to detect the expressions of β-actin, proliferating cell nuclear antigen (PCNA), Bax, Bcl-2, Wnt-3a, Beta-catenin (β-catenin), serine protein kinase 3β (p-GSK-3β), glycogen synthase kinase-3β (GSK-3β) and c-myc.ResultsDifferent concentrations of telmisartan treatment inhibited the proliferation activity, colony-formation rate and migration of A549 cells, and reduced the expression of PCNA in a concentration-dependent manner. Telmisartan treatment promoted the apoptosis of A549 cells, significantly increased the expression of pro-apoptotic protein Bax and decreased the expression of anti-apoptotic protein Bcl-2. The expression levels of Wnt-3a, β-catenin, p-GSK-3β, and c-myc in A549 cells increased after treatment with telmisartan, while the expression levels of GSK-3β decreased.ConclusionTelmisartan may play a role in the proliferation, migration and apoptosis of non-small cell lung cancer A549 cells, and inhibiting the Wnt/β-catenin signaling pathway may be one of the mechanisms.
ObjectiveTo construction the telmisartan/collagen/polycaprolactone (PCL) nerve conduit and assess its effect on repairing sciatic nerve defect in rats. Methods The 60% collagen/hexafluoroisopropanol (HFIP) solution and 40% PCL/HFIP solution were prepared and mixed (collagen/PCL solution). Then the 0, 5, 10, and 20 mg of telmisartan were mixed with the 10 mL collagen/PCL solution, respectively. Telmisartan/collagen/PCL nerve conduits were fabricated via high voltage electrospinning technology. The structure of nerve conduit before and after crosslinking was observed by using scanning electron microscope (SEM). The drug release efficiency was detected by in vitro sustained release method. RAW264.7 cells were cultured with lipopolysaccharide to induce inflammation, and then co-cultured with nerve conduits loaded with different concentrations of telmisartan for 24 hours. The mRNA expressions of inducible nitric oxide synthase (iNOS) and Arginase 1 (Arg-1) were detected by using real-time fluorescence quantitative PCR. Forty adult Wistar rats were randomly divided into 4 groups (n=10). After preparing 15-mm-long sciatic nerve defect, the defect was repaired by cross-linked nerve conduits loaded with 0, 5, 10, and 20 mg telmisartan in groups A, B, C, and D, respectively. After operation, the general condition of rats was observed after operation; the sciatic function index (SFI) was tested; the bridging between the nerve conduit and sciatic nerve, and the integrity of nerve conduit were observed; the tissue growth in nerve conduit and material degradation were observed by HE staining; the expressions of CD86 (M1 macrophage marker), CD206 (M2 macrophage marker), myelin basic protein (MBP), and myelin protein 0 (P0) in new tissues were also observed by immunohistochemical staining; the expressions of neurofilament 200 (NF-200) and S-100β in new tissues were assessed by immunofluorescence staining. Results The general observation showed that the inner diameter of the nerve conduit was 1.8 mm and the outer diameter was 2.0 mm. After cross-linking by genipin, the nanofiber became thicker and denser. The drug release test showed that the telmisartan loaded nerve conduit could be released gradually. With the increase of telmisartan content in nerve conduit, the iNOS mRNA expression decreased and the Arg-1 mRNA expression increased; and the differences between 20 mg group and other groups were significant (P<0.05). In vivo experiment showed that all animals in each group survived until the completion of the experiment. The SFI was significantly higher in groups C and D than in groups A and B at different time points (P<0.05) and in group D than in group C at 6 months after operation (P<0.05). HE staining showed that there were significantly more new tissues in the middle of the nerve conduit in group D after operation than in other groups. Immunohistochemical staining showed that CD86 and CD206 stainings were positive in each group at 1 month after operation, among which group D had the lowest positive rate of CD86 and the highest positive rate of CD206, and there were significant differences in the positive rate of CD206 between group D and groups A, B, and C (P<0.05); the MBP and P0 stainings were positive in groups C and D at 6 months, and the positive rate in group D was significantly higher than that in group C (P<0.05). Immunofluorescence staining showed that the NF-200 and S-100β expressions in group D were significantly higher than those in other groups. ConclusionTelmisartan/collagen/PLC nerve conduit can promote the sciatic nerve defect repair in rats through promoting the polarization of M1 macrophages to M2 macrophages, and the nerve conduit loaded with20 mg telmisartan has the most significant effect.