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Realtime xCELLigence analysis (RTCA) is a new cell detection technology to continuously monitor, record and analyze a variety of information generated by cell activity. In drug research, it plays an important role in assessing myocardial toxicity and cell biological activity. Here, we first introduce the underlying mechanisms and characteristics of RTCA. Then we review the applications of RTCA in the research of myocardial toxicity and cell biological activity, to provides the fundamental baseline for understanding and exploiting RTCA. With the real-time, unlabeled, non-invasive, high throughput, and high accuracy features, RTCA not only promotes drug research and development, but also has a broad and good application prospect in other fields.
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Preparaciones FarmacéuticasRESUMEN
<b>Objective::To study the protective effect and mechanism of Qidong Yixin oral liquid on doxorubicin-induced myocardial toxicity in mice. <b>Method::Ninety male ICR mice were randomly divided into normal group, model(DOX) group, DOX+ Qidong Yixin oral liquid group (9.55, 23.88, 47.75 g·kg<sup>-1</sup>) and high dose group (47.75 g·kg<sup>-1</sup>) with 15 mice in each group. The normal group and model group were given pure water by gavage, and each dose group of Qidong Yixin oral liquid was given different doses of Qidong Yixin oral liquid once a day for 21 days. On the seventh day, normal saline was injected into the abdominal cavity of the normal group and the high dose group of Qidong Yixin oral liquid. Doxorubicin was injected into the abdominal cavity of the other groups (15 mg·kg<sup>-1</sup>). After 21 days, the weight and heart weight of mice were weighed and cardiac index was calculated. Serum was taken for the detection of lactate dehydrogenase (LDH), creatine kinase (CK), aspartate aminotransferase (AST). Heart was taken for hematoxylin-eosin (HE) staining, superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), catalase (CAT) in myocardial tissue were detected. The expression of nuclear factor NF-E2 related factor (Nrf2) and heme oxygenase-1 (HO-1) were detected by Western blot. <b>Result::Compared with normal group, adriamycin could significantly reduce the body weight of mice (<italic>P</italic><0.01), increase the activities of LDH, CK and AST in serum(<italic>P</italic><0.01), and decrease the activities of antioxidant enzymes (<italic>P</italic><0.01). Compared with DOX group, high dose Qidong Yixin oral liquid could significantly increase the weight of mice (<italic>P</italic><0.05, <italic>P</italic><0.01), decrease the level of myocardial three enzymes(<italic>P</italic><0.01), increase the activity of antioxidant enzymes(<italic>P</italic><0.05, <italic>P</italic><0.01), and increase the expression of Nrf2 and HO-1(<italic>P</italic><0.01). <b>Conclusion::Qidong Yixin oral liquid has a good protective effect on doxorubicin myocardial toxicity. Its mechanism may be related to activating Nrf2/HO-1 signaling pathway and alleviating oxidative stress injury.
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Objective To investigate the protective effect of FUC on adriamycin (ADR) - induced myocardial cell toxicity. Methods Using DPPH FUC method to study the scavenging effect on free radicals play a protective role of H9C2, MTT method is used to study the cytotoxicity of FUC on ADR induced by the H9C2 cell morphological changes were observed by AO/EB staining, the expression of H9C2 in cells of ROS levels and H9C2 cell apoptosis related protein Carboxy-DCFDA Western and Blotting detection method. Results DPPH assay showed that FUC has strong scavenging of oxygen free radicals, FUC to play a good protective effect H9C2 cytotoxicity caused by ADR and mechanism of apoptosis in H9C2 cells were cytotoxic FUC protective effect of H9C2 on ADR induced by the reduced ADR induced increase, elevated levels of reactive oxygen species that caused by ADR the H9C2 cells and H9C2 cells apoptosis protein Caspase-8 Cleaved Cas-pase-3, Cleaved and downreguLation of PARP upreguLation inhibited. Conclusion The protective effect of FUC on myocardial cell toxicity caused by ADR is played by oxidative stress in myocardial cells by antioxidant activity has its own ADR induced inhibition of blocked ADR induced myocardial cell activation of Caspase-8 pathway, thereby effectively inhibit ADR induced Cas-pase-3 activation and PARP shear this continuous process to achieve.
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At present, there is no specific antidote for local anesthetic toxicity, which seriously hindered therapeutic efficts of clinical treatment. It is increasingly urgent for finding find the effective antidote to local anesthetic. This article at-tempts to interpret the molecular pharmacological mechanism from fat pool, energy metabolism, NO, ion channel and solubili-zation for the role of fatty acids in reversal of myocardial toxicity of local anesthetics. And the different characteristics of the structure and function of nano liposome and fat emulsion were compared.