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Zheng‐Yu Cheng Fu‐Shin Chueh Shu‐Fen Peng Chia‐Hsin Lin Chao‐Lin Kuo Wen‐Wen Huang Po‐Yuan Chen Tzong‐Der Way Jing‐Gung Chung 《Environmental toxicology》2020,35(9):911-921
Leukemia is one of the major diseases causing cancer‐related deaths in the young population, and its cure rate is unsatisfying with side effects on patients. Fluorouracil (5‐FU) is currently used as an anticancer drug for leukemia patients. Casticin, a natural polymethoxyflavone, exerts anticancer activity against many human cancer cell lines in vitro, but no other reports show 5‐FU combined with casticin increased the mouse leukemia cell apoptosis in vitro. Herein, the antileukemia activity of 5‐FU combined with casticin in WEHI‐3 mouse leukemia cells was investigated in vitro. Treatment of two‐drug combination had a higher decrease in cell viability and a higher increase in apoptotic cell death, the level of DNA condensation, and the length of comet tail than that of 5‐FU or casticin treatment alone in WEHI‐3 cells. In addition, the two‐drug combination has a greater production rate of reactive oxygen species but a lower level of Ca2+ release and mitochondrial membrane potential (ΔΨm) than that of 5‐FU alone. Combined drugs also induced higher caspase‐3 and caspase‐8 activities than that of casticin alone and higher caspase‐9 activity than that of 5‐FU or casticin alone at 48 hours treatment. Furthermore, 5‐FU combined with casticin has a higher expression of Cu/Zn superoxide dismutase (SOD [Cu/Zn]) and lower catalase than that of 5‐FU or casticin treatment alone. The combined treatment has higher levels of Bax, Endo G, and cytochrome C of proapoptotic proteins than that of casticin alone and induced lower levels of B‐cell lymphoma 2 (BCL‐2) and BCL‐X of antiapoptotic proteins than that of 5‐FU or casticin only. Furthermore, the combined treatment had a higher expression of cleaved poly (ADP‐ribose) polymerase (PARP) than that of casticin only. Based on these findings, we may suggest that 5‐FU combined with casticin treatment increased apoptotic cell death in WEHI‐3 mouse leukemia cells that may undergo mitochondria and caspases signaling pathways in vitro. 相似文献
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The effects of intravenous verapamil on the electrocardiogram in 15 patients with heart disease in sinus rhythm and in 44 patients with supraventricular and ventricular tachyarrhythmias were evaluated. Verapamil prolonged the P-R interval without effect on the QRS duration or the Q-Tc interval. In patients with atrial flutter and fibrillation, A-V block was increased, with slowing of the ventricular rate, in almost all cases but sinus rhythm was restored in only 1 of 12 patients in atrial fibrillation and in 2 of the 11 patients with flutter. Verapamil had no effect in 3 patients with atrial fibrillation complicating WPW syndrome; in 1 of 5 patients with ventricular tachycardia it caused reversion to sinus rhythm. Sinus rhythm was restored promptly by verapamil in 13 of 17 patients with paroxysmal supraventricular tachycardias; in 2 others, sinus rhythm became established 1 to 2 hours after administration of the drug. Transient hypotension, not requiring treatment, was the only side effect noted but not in the patients with supraventricular tachycardias, in whom blood pressure generally increased after reversion to sinus rhythm by verapamil. 相似文献
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[目的]探讨伊立替康联合化疗治疗原发性肝癌的疗效和毒性反应。[方法]2004年9月-2007年3月于大连医科大学第二临床学院肿瘤科确诊为原发性肝癌的患者21例,采用依立替康(CPT-11)联合5-FU、DDP化疗,其中A组11例,CPT-11100 mg,DDP 60 mg,5-FU1000 mg,1次/d,经肝动脉灌注,B组10例,CPT-11100 mg,第1、8、15天,DDP75 mg/m^2,静脉滴注,5-FU300 mg/d,1次/d,连续7 d,持续静脉灌注,全部21-28 d为1周期。评价指标:有效率、临床获益率(完全缓解+部分缓解+稳定),AFP下降情况、mTTP、毒性反应。[结果]A组疗效均为稳定,临床获益率100%,AFP下降者占50%,mTTP为5个月,B组1例部分缓解(10%),5例稳定(50%),临床获益率60%,AFP下降者20%,mTTP为5个月。毒性反应主要表现为骨髓毒性、肝功能毒性、迟发性腹泻。[结论]CPT-11联合化疗对于原发性肝癌有一定的疗效,与常规治疗相比,疗效相当,但在临床获益率和中位肿瘤进展时间方面显示一定的优势,毒性反应较轻微。其中,肝动脉灌注给药较静脉给药临床获益率较高,毒性反应较低,中位肿瘤进展时间相当,初步认为肝动脉灌注化疗优于静脉全身化疗。但对于无肝动脉灌注治疗指征或已出现血行转移的原发性肝癌患者采用静脉化疗,亦可获得一定的有效率,中位肿瘤进展时间延长,患者可明显获益。 相似文献
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Understanding why persons with human immunodeficiency virus (HIV) have accelerated atherosclerosis and its sequelae, including coronary artery disease (CAD) and myocardial infarction, is necessary to provide appropriate care to a large and aging population with HIV. In this review, we delineate the diverse pathophysiologies underlying HIV-associated CAD and discuss how these are implicated in the clinical manifestations of CAD among persons with HIV. Several factors contribute to HIV-associated CAD, with chronic inflammation and immune activation likely representing the primary drivers. Increased monocyte activation, inflammation, and hyperlipidemia present in chronic HIV infection also mirror the pathophysiology of plaque rupture. Furthermore, mechanisms central to plaque erosion, such as activation of toll-like receptor 2 and formation of neutrophil extracellular traps, are also abundant in HIV. In addition to inflammation and immune activation in general, persons with HIV have a higher prevalence than uninfected persons of traditional cardiovascular risk factors, including dyslipidemia, hypertension, insulin resistance, and tobacco use. Antiretroviral therapies, although clearly necessary for HIV treatment and survival, have had varied effects on CAD, but newer generation regimens have reduced cardiovascular toxicities. From a clinical standpoint, this mix of risk factors is implicated in earlier CAD among persons with HIV than uninfected persons; whether the distribution and underlying plaque content of CAD for persons with HIV differs considerably from uninfected persons has not been definitively studied. Furthermore, the role of cardiovascular risk estimators in HIV remains unclear, as does the role of traditional and emerging therapies; no trials of CAD therapies powered to detect clinical events have been completed among persons with HIV. 相似文献