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Fujian Medical University
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北大核心 CSTPCD CSCD CA CBST
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摘要:目的:探讨心率减速力(DC)在预测表阿霉素对恶性肿瘤患者心脏毒性中的价值。方法:回顾性分析广西医科大学附属肿瘤医院经病理确诊为恶性肿瘤并用含表阿霉素方案化疗的140例患者临床资料,收集所有患者化疗前后CK-MB、cTnI、动态心电图资料,根据计算出的DC值分为DC>4.5 ms组和DC≤4.5 ms组,对比两组含表阿霉素方案患者化疗前、化疗2、4个周期后CK-MB、cTnI水平及动态心电图平均心率、室上性及室性心律失常计数。结果:两组患者化疗前相关临床病理资料比较,差异无统计学意义(P>0.05);化疗4个周期后DC≤4.5 ms组的血清CK-MB和cTnⅠ浓度与化疗前差值的均数高于DC>4.5 ms组,差异有统计学意义(P<0.05);化疗2、4个周期后DC≤4.5 ms组的平均心率、室上性心律失常及室性心律失常计数与化疗前差值的均数高于DC>4.5 ms组,差异均有统计学意义(P<0.05);化疗后DC≤4.5 ms组中23例患者cTnⅠ异常升高,且cTnⅠ升高患者与cTnⅠ正常患者在化疗前CK-MB和cTnⅠ浓度、平均心率、室上性心律失常及室性心律失常比较,差异无统计学意义,而cTnⅠ升高患者的DC值明显低于cTnⅠ正常患者,差异有统计学意义(P<0.05)。结论:表阿霉素导致心脏毒性发生的风险随患者DC值下降而增加,化疗前检测DC值能较好地预测患者发生表阿霉素心脏毒性的风险。...
摘要:AIM: To investigate the effect of curcumin on tert-butyl hydroperoxide (t-BHP)-induced oxidative damage in rat cortical neurons and to explore the possible mechanism. METHODS: Primary cultured rat cortical neurons were performed in vitro and cell viability was measured by MTT assay. DNA fragmentation was used to evaluate cell apoptosis. Intracellular reactive oxygen species (ROS) and mitochondrial membrane potential (△ψm) was determined by flow cytometric assay. Cellular glutathione (GSH) content was measured by spectrophotometer. Bcl-2family proteins, cytochrome c, cleaved caspase-3, and poly (ADP-ribose) polymerase (PARP) were detected by Western blot. RESULTS: Exposure of tBHP 100μmol/L to neurons for 60 min resulted in Aψm loss and cytochrome c release from mitochondria and subsequent activation of caspase-3 and PARP cleavation, and cell apoptosis.After removal of tBHP and then further treatment with curcumin (2.5-20μmol/L) for 18 h, curcumin abrogated △ψm loss and cytochrome c release, blocked activation of caspase 3, and altered the expression of Bcl-2 family.Further curcumin treatment also prevented cellular GSH and decreased intracellular ROS generation markedly.Curcumin eventually attenuated tBHP-induced apoptosis in cortical neurons. CONCLUSION: Curcumin may attenuate oxidative damages in cortical neurons by reducing intracellular production of ROS and protecting mitochondria from oxidative damage....
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