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| 1 | Cardiotoxicity of 5-fluorouracil and capecitabine in Chinese patients: a prospective study显示文摘Background:5-Fluorouracil(5-FU)and capecitabine-associated cardiotoxicity ranging from asymptomatic electro-cardiography(ECG)abnormalities to severe myocardial infarction has been reported in a number of studies,but such cardiotoxicity in Chinese patients with malignant diseases has not been investigated to date.In the present study,we aimed to prospectively evaluate the incidence rates and clinical manifestations of 5-FU-and capecitabine-associated cardiotoxicity in cancer patients recruited from multiple centers in China.Methods:Among the 527 patients who completed the study,196 received 5-FU-based chemotherapy and 331 received capecitabine-based chemotherapy as either first-line or adjuvant therapy.Adverse events were reported during the treatment and up to 28 days of follow-up.Outcome measures included ECG,myocardial enzymes,cardiac troponin,brain natriuretic peptide and echocardiography.Univariate analysis and logistic regression were performed for subgroup analysis and identification of significant independent variables that are associated with cardiotoxicity of both agents.Results:In total,161 of 527 patients(30.6%)experienced cardiotoxicity.The incidence rate of cardiotoxicity was 33.8%(112/331)in the capecitabine group,which was significantly higher than the rate of 25%(49/196)in the 5-FU group(P=0.0042).110/527 patients(20.9%)suffered arrhythmia,105/527(19.9%)developed ischemic changes,while only 20/527 patients(3.8%)presented heart failure and 6/527 patients(1.1%)had myocardial infarction.Pre-existing cardiac disease,hypertension,capecitabine-based chemotherapy and duration of treatment were identified as sig-nificant risk factors associated with cardiotoxicity.The odds ratio were 15.7(prior history of cardiac disease versus no history),1.86(capecitabine versus 5-FU),1.06(5-8 versus 1-4 chemotherapy cycles)and 1.58(hypertension versus no hypertension),respectively.Conclusions:Cardiotoxicity induced by fluoropyrimidines in the Chinese population may be underestimated in clini-cal practice.Close monitoring of patients is recommended,especially for those patients at high risk for cardiotoxicity.Possible risk factors are duration of treatment,capecitabine-based chemotherapy,pre-existing cardiac diseases and hypertension.Trial registration This study was initiated on January 22,2014 and has been retrospectively registered with the registra-tion number ChiCTR1800015434 . | Jianjun Peng Chao Dong Chang Wang Weihua Li Hao Yu Min Zhang Qun Zhao Bo Zhu Jun Zhang Wenliang Li Fenghua Wang Qiong Wu Wenhao Zhou Ying Yuan Meng Qiu Gong Chen | 2018 | Cancer Communications2018，38，1： | 23 |
| 2 | Enhanced myocardial fluorodeoxyglucose uptake following Adriamycin-based therapy: Evidence of early chemotherapeutic cardiotoxicity?显示文摘AIM: To analyze changes in myocardial glucose metabolism using fluorodeoxyglucose (FDG)-positron emission tomography (PET) in patients treated with adriamycin and to investigate the clinical significance of these changes.METHODS: Considering that FDG-PET scanning has the ability to show changes in glucose metabolism in the myocardium, we retrospectively analyzed the FDGPET studies of 18 lymphoma patients treated with adriamycin-based chemotherapy in both the preand posttherapy setting. Cardiac contractile parameters such as left ventricular ejection fraction were not available for correlation in all patients due to the short duration and the level of cumulative dose administered in these patients during the time of the follow-up FDG-PET study. The change in myocardial glucose utilization was estimated by change in standard uptake values (SUV) in the myocardium.RESULTS: We observed a significant change in SUVmean values in the myocardium (defined as more than change in cardiac SUVmean between pre-and post-chemotherapy PET) in 1 patients, whereas 6 patients did not show any significant cardiac FDG uptake in both preand post-therapy PET scans. Patients were divided into three groups based on the changes observed in myocardial tracer uptake on the followup 18 F-FDG-PET study. Group A (n = 8): showed an increase in cardiac 18 F-FDG uptake in the post-therapy scan compared to the baseline scan carried out prior to starting adriamycin-based chemotherapy. Group B (n = 6): showed no significant cardiac 18 F-FDG uptake in post-therapy and baseline PET scans, and group C (n = 4): showed a fall in cardiac 18 F-FDG uptake in the posttherapy scan compared to the baseline scan. Mean cumulative adriamycin dose (in mg/m 2 ) received during the time of the follow-up FDG-PET study was 256. 25, 250 and 137.5, respectively.CONCLUSION: Our study shows three different trends in the change in myocardial glucose metabolism in patients undergoing adriamycin-based chemotherapy. A further prospective study with prolonged follow-up of ventricular function is warranted to explore the significance of enhanced FDG uptake as a marker of early identification of adriamycin-induced cardiotoxicity. | Chaitanya Borde Purushottam Kand Sandip Basu | 2012 | World Journal of Radiology2012，4，5： | 9 |
| 3 | IGF1-PI3K-induced physiological cardiac hypertrophy:Implications for new heart failure therapies,biomarkers,and predicting cardiotoxicity显示文摘Heart failure represents the end point of a variety of cardiovascular diseases.It is a growing health burden and a leading cause of death worldwide.To date,limited treatment options exist for the treatment of heart failure,but exercise has been well-established as one of the few safe and effective interventions,leading to improved outcomes in patients.However,a lack of patient adherence remains a significant barrier in the implementation of exercise-based therapy for the treatment of heart failure.The insulin-like growth factor 1(IGF1)phosphoinositide 3-kinase(PI3K)pathway has been recognized as perhaps the most critical pathway for mediating exercisedinduced heart growth and protection.Here,we discuss how modulating activity of the IGF1PI3K pathway may be a valuable approach for the development of therapies that mimic the protective effects of exercise on the heart.We outline some of the promising approaches being investigated that utilize PI3K-based therapy for the treatment of heart failure.We discuss the implications for cardiac pathology and cardiotoxicity that arise in a setting of reduced PI3K activity.Finally,we discuss the use of animal models of cardiac health and disease,and genetic mice with increased or decreased cardiac PI3K activity for the discovery of novel drug targets and biomarkers of cardiovascular disease. | Sebastian Bass-Stringer Celeste M.K.Tai Julie R.McMullen | 2021 | Journal of Sport and Health Science2021，10，6： | 9 |
| 4 | Chrysophanol protects against doxorubicin-induced cardiotoxicity by suppressing cellular PARylation显示文摘The clinical application of doxorubicin(DOX) in cancer chemotherapy is limited by its lifethreatening cardiotoxic effects. Chrysophanol(CHR), an anthraquinone compound isolated from the rhizome of Rheum palmatum L., is considered to play a broad role in a variety of biological processes.However, the effects of CHR’s cardioprotection in DOX-induced cardiomyopathy is poorly understood. In this study, we found that the cardiac apoptosis, mitochondrial injury and cellular PARylation levels were significantly increased in H9 C2 cells treated by Dox, while these effects were suppressed by CHR. Similar results were observed when PARP1 activity was suppressed by its inhibitors 3-aminobenzamide(3 AB)and ABT888. Ectopic expression of PARP1 effectively blocked this CHR’s cardioprotection against DOX-induced cardiomyocyte injury in H9 C2 cells. Furthermore, pre-administration with both CHR and 3 AB relieved DOX-induced cardiac apoptosis, mitochondrial impairment and heart dysfunction in Sprague–Dawley rat model. These results revealed that CHR protects against DOX-induced cardiotoxicity by suppressing cellular PARylation and provided critical evidence that PARylation may be a novel target for DOX-induced cardiomyopathy. | Jing Lu Jingyan Li Yuehuai Hu Zhen Guo Duanping Sun Panxia Wang Kaiteng Guo Dayue Darrel Duan Si Gao Jianmin Jiang Junjian Wang Peiqing Liu | 2019 | Acta Pharmaceutica Sinica B2019，9，4： | 8 |
| 5 | Isorhapontigenin protects against doxorubicin-induced cardiotoxicity via increasing YAP1 expression显示文摘As an effective anticancer drug, the clinical limitation of doxorubicin(Dox) is the time-and dose-dependent cardiotoxicity. Yes-associated protein 1(YAP1) interacts with transcription factor TEA domain 1(TEAD1) and plays an important role in cell proliferation and survival. However, the role of YAP1 in Dox-induced cardiomyopathy has not been reported. In this study, the expression of YAP1 was reduced in clinical human failing hearts with dilated cardiomyopathy and Dox-induced in vivo and in vitro cardiotoxic model. Ectopic expression of Yap1 significantly blocked Dox-induced cardiomyocytes apoptosis in TEAD1 dependent manner. Isorhapontigenin(Isor) is a new derivative of stilbene and responsible for a wide range of biological processes. Here, we found that Isor effectively relieved Doxinduced cardiomyocytes apoptosis in a dose-dependent manner in vitro. Administration with Isor(30 mg/kg/day, intraperitoneally, 3 weeks) significantly protected against Dox-induced cardiotoxicity in mice. Interestingly, Isor increased Dox-caused repression in YAP1 and the expression of its target genes in vivo and in vitro. Knockout or inhibition of Yap1 blocked the protective effects of Isor on Dox-induced cardiotoxicity. In conclusion, YAP1 may be a novel target for Dox-induced cardiotoxicity and Isor might be a new compound to fight against Dox-induced cardiotoxicity by increasing YAP1 expression. | Panxia Wang Minghui Wang Yuehuai Hu Jianxing Chen Yanjun Cao Cui Liu Zhongkai Wu Juan Shen Jing Lu Peiqing Liu | 2021 | Acta Pharmaceutica Sinica B2021，11，3： | 7 |
| 6 | Bufalin-induced cardiotoxicity: new findings into mechanisms显示文摘Bufalin is one of the main pharmacological and toxicological components of Venenum Bufonis and many traditional Chinese medicine preparations.The cardiotoxicity clearly limits its application to patients living in countries.Hence,an investigation of its toxicological mechanism is helpful for new drug development and treatment of the related clinical adverse reactions.We investigate the cardiotoxicity of bufalin using human induced pluripotent stem cells-derived cardiomyocytes(hiPSC-CMs)(0.003–0.1μmol·L–1),human induced pluripotent stem cells-derived cardiomyocytes(hiPSC-CMs)(0.03–0.3μmol·L–1)and eight human cardiac ion channel currents(0.01–100μmol·L–1)combined with an impedance-based bioanalytical and patch clamp method.Biphasic effect of bufalin on the contractility in hiPSC-CMs,which has been shown to strengthen myocardial contractility,accelerate conduction,and increase beating rate at the earlier stage of administration,whereas weakened myocardial contractility,abolished conduction,and ceased beating rate at the later stage of administration.Bufalin decreased the action potential duration(Action potential duration at 30%,50%and 90%repolarization),cardiac action potential amplitude,and maximal depolarization rate and depolarized the resting membrane potential of hiPSC-CMs.Spontaneous beating rates of hiPSC-CMs were markedly increased at 0.03μmol·L–1,while were weakened at 0.3μmol·L–1 after application.Bufalin blocks INav1.5 in a concentration-dependent manner with half maximal inhibitory concentration of 74.5μmol·L–1.Bufalin respectively increased the late sodium current and Na+-Ca2+exchange current with a concentration for 50%of maximal effect of 2.48 and 66.06μmol·L–1 in hiPSC-CMs.Whereas,bufalin showed no significant effects on other cardiac ion channel currents.The enhancement of the late sodium current is one of the main mechanism for cardiotoxicity of bufalin. | LI Min WANG Xi-Jie ZHAO Qi WANG Jia-Xian XING Hong-Yan ZHANG Yi-Zhe ZHANG Xue-Xia ZHI Yang-Yang LI Hua MA Jing | 2020 | Chinese Journal of Natural Medicines2020，18，7： | 5 |
| 7 | The association between early-onset cardiac events caused by neoadjuvant or adjuvant chemotherapy in triple-negative breast cancer patients and some novel autophagy-related polymorphisms in their genomic DNA: a real-world study显示文摘Background:An increasing number of cancer patients die of cardiovascular diseases.The cardiotoxicity of chemo-therapy is particularly important in triple-negative breast cancer(TNBC)with limited therapeutic options.Cardiac autophagy is an important mechanism of cardiotoxicity.This research was aimed to investigate the cardiotoxicity of chemotherapy in TNBC,screen the susceptible population,and determine the relationship between cardiotoxicity and autophagy-related polymorphisms.Methods:From a total of 2450 stage I-III TNBC patients,147 met the inclusion criteria and finally recruited.Electro-cardiography(ECG)was performed before most chemotherapy cycles,and echocardiography(UCG)was performed according to clinical needs.All ECG and UCG records were re-interpreted by cardiologists at the National Center for Cardiovascular Disease,Fuwai Hospital.According to the National Center for Biotechnology Information and the Catalog of Somatic Mutations in Cancer database,we selected 25 single nucleotide polymorphisms(SNPs)related to autophagy and genotyped the 147 TNBC patients.Paired-sample T tests,Chi squared tests,and logistic regression models were employed for the analysis.Results:Only 46(31.3%)patients had normal ECG records after every chemotherapy cycle.Among the 16 patients who underwent UCG,2(12.5%)had a reversible decrease of left ventricular ejection fraction.The use of anthracyclines and excessive alcohol consumption were risk factors of ECG abnormalities.With the continuation of chemotherapy,heart rate gradually increased.Anthracyclines were associated with QRS duration abnormalities(P=0.043).After genotyping for 25 autophagy-related SNPs,we found that the G allele of autophagy-related 13(ATG13)rs10838611 was significantly associated with ECG abnormalities(odds ratio=2.258,95%confidence interval=1.318-3.869;P=0.003).Conclusion:ECG abnormalities caused by chemotherapy are common in the real world.Autophagy-related SNPs are associated with chemotherapy-induced cardiotoxicity,thereby providing new evidence for autophagy as a cause of chemotherapy-induced cardiac damage. | Binliang Liu Tao An Meiying Li Zongbi Yi Chunxiao Li Xiaoying Sun Xiuwen Guan Lixi Li Yanfeng Wang Yuhui Zhang Binghe Xu Fei Ma Yixin Zeng | 2018 | Cancer Communications2018，38，1： | 5 |
| 8 | Antipsychotics cardiotoxicity:What's known and what's next显示文摘Chronic use of antipsychotic medications entails a dilemma between the benefit of alleviating psychotic symptoms and the risk of troubling,sometimes lifeshortening adverse effects.Antipsychotic-induced cardiotoxicity is one of the most life-threatening adverse effects that raises widespread concerns.These cardiotoxic effects range from arrhythmia to heart failure in the clinic,with myocarditis/cardiomyopathy,ischemic injuries,and unexplained cardiac lesions as the pathological bases.Multiple mechanisms have been proposed to underlie antipsychotic cardiotoxicity.This review aims to summarize the clinical signs and pathological changes of antipsychotic cardiotoxicity and introduce recent progress in understanding the underlying mechanisms at both the subcellular organelle level and the molecular level.We also provide an up-to-date perspective on future clinical monitoring and therapeutic strategies for antipsychotic cardiotoxicity.We propose that third-generation antipsychotics or drug adjuvant therapy,such as cannabinoid receptor modulators that confer dual benefits—i.e.,alleviating cardiotoxicity and improving metabolic disorders—deserve further clinical evaluation and marketing. | Xiao-Qing Li Xin-Ru Tang Li-Liang Li | 2021 | World Journal of Psychiatry2021，11，10： | 5 |
| 9 | Induced pluripotent stem cells for therapy personalization in pediatric patients:Focus on drug-induced adverse events显示文摘Adverse drug reactions(ADRs)are major clinical problems,particularly in special populations such as pediatric patients.Indeed,ADRs may be caused by a plethora of different drugs leading,in some cases,to hospitalization,disability or even death.In addition,pediatric patients may respond differently to drugs with respect to adults and may be prone to developing different kinds of ADRs,leading,in some cases,to more severe consequences.To improve the comprehension,and thus the prevention,of ADRs,the set-up of sensitive and personalized assays is urgently needed.Important progress is represented by the possibility of setting up groundbreaking patient-specific assays.This goal has been powerfully achieved using induced pluripotent stem cells(iPSCs).Due to their genetic and physiological species-specific differences and their ability to be differentiated ideally into all tissues of the human body,this model may be accurate in predicting drug toxicity,especially when this toxicity is related to individual genetic differences.This review is an up-to-date summary of the employment of iPSCs as a model to study ADRs,with particular attention to drugs used in the pediatric field.We especially focused on the intestinal,hepatic,pancreatic,renal,cardiac,and neuronal levels,also discussing progress in organoids creation.The latter are three-dimensional in vitro culture systems derived from pluripotent or adult stem cells simulating the architecture and functionality of native organs such as the intestine,liver,pancreas,kidney,heart,and brain.Based on the existing knowledge,these models are powerful and promising tools in multiple clinical applications including toxicity screening,disease modeling,personalized and regenerative medicine. | Elena Genova Federica Cavion Marianna Lucafò Luigina De Leo Marco Pelin Gabriele Stocco Giuliana Decorti | 2019 | World Journal of Stem Cells2019，11，12： | 4 |
| 10 | Managing cardiotoxicity associated with immune checkpoint inhibitors显示文摘Immuno-oncology is a fast evolving field of cancer therapy and immune checkpoint inhibitors (ICIs) are clearly a breakthrough in this field. Cardiotoxicity with conventional anti-cancer therapies has been well studied in the past and clear guidelines for management of these side effects are available in the literature. However, cardiotoxicity with novel agents such as ICIs has been fairly under-reported and/or underestimated and we are yet to formulate clear guidelines for management of these rare side effects. In the last few years, there has been an overall increase in the number of cases of cardiotoxicity related to ICIs. In this literature review, we describe the mechanism of action of the most widely used ICIs and their related cardiotoxicities. The increase in number of case reports about the potential of cardiotoxicities with these novel agents clearly indicates the need for a new insight into the field of cardio-immuno-oncology. | Sireesha Upadhrasta Hadi Elias Keval Patel Lei Zheng | 2019 | Chronic Diseases and Translational Medicine2019，5，1： | 4 |
| 11 | Nuclear imaging in detection and monitoring of cardiotoxicity显示文摘Cardiotoxicity as a result of cancer treatment is a novel and serious public health issue that has a significant impact on a cancer patient’s management and outcome.The coexistence of cancer and cardiac disease in the same patient is more common because of aging population and improvements in the efficacy of antitumor agents.Left ventricular dysfunction is the most typical manifestation and can lead to heart failure.Left ventricular ejection fraction measurement by echocardiography and multigated radionuclide angiography is the most common diagnostic approach to detect cardiac damage,but it identifies a late manifestation of myocardial injury.Early non-invasive imaging techniques are needed for the diagnosis and monitoringof cardiotoxic effects.Although echocardiography and cardiac magnetic resonance are the most commonly used imaging techniques for cardiotoxicity assessment,greater attention is focused on new nuclear cardiologic techniques,which can identify high-risk patients in the early stage and visualize the pathophysiologic process at the tissue level before clinical manifestation.The aim of this review is to summarize the role of nuclear imaging techniques in the non-invasive detection of myocardial damage related to antineoplastic therapy at the reversible stage,focusing on the current role and future perspectives of nuclear imaging techniques and molecular radiotracers in detection and monitoring of cardiotoxicity. | Carmen D’Amore Paola Gargiulo Stefania Paolillo Angela Maria Pellegrino Tiziana Formisano Antonio Mariniello Giuseppe DellaRatta Elisabetta Iardino Marianna D’Amato Lucia La Mura Irma Fabiani Flavia Fusco Pasquale Perrone Filardi | 2014 | World Journal of Radiology2014，6，7： | 2 |
| 12 | Noncoding RNAs in doxorubicin-induced cardiotoxicity and their potential as biomarkers and therapeutic targets显示文摘Anthracyclines,such as doxorubicin(DOX),are well known for their high efficacy in treating multiple cancers,but their clinical usage is limited due to their potential to induce fatal cardiotoxicity.Such detrimental effects significantly impact the overall physical condition or even induce the morbidity and mortality of cancer survivors.Therefore,it is extremely important to understand the mechanisms of DOX-induced cardiotoxicity to develop methods for the early detection of cytotoxicity and therapeutic applications.Studies have shown that many molecular events are involved in DOX-induced cardiotoxicity.However,the precise mechanisms are still not completely understood.Recently,noncoding RNAs(ncRNAs)have been extensively studied in a diverse range of regulatory roles in cellular physiological and pathological processes.With respect to their roles in DOX-induced cardiotoxicity,microRNAs(miRNAs)are the most widely studied,and studies have focused on the regulatory roles of long noncoding RNAs(lncRNAs)and circular RNAs(circRNAs),which have been shown to have significant functions in the cardiovascular system.Recent discoveries on the roles of ncRNAs in DOX-induced cardiotoxicity have prompted extensive interest in exploring candidate ncRNAs for utilization as potential therapeutic targets and/or diagnostic biomarkers.This review presents the frontier studies on the roles of ncRNAs in DOX-induced cardiotoxicity,addresses the possibility and prospects of using ncRNAs as diagnostic biomarkers or therapeutic targets,and discusses the possible reasons for related discrepancies and limitations of their use. | Hong-ge Fa Wen-guang Chang Xue-juan Zhang Dan-dan Xiao Jian-xun Wang | 2021 | Acta Pharmacologica Sinica2021，42，4： | 2 |
| 13 | Fluoropyrimidine-induced cardiotoxicity显示文摘Cardio-oncology is a discipline based on early screening,monitoring,and treating chemotherapy-induced cardiotoxicity.There are many chemotherapeutics known for their cardiac toxic effects,including fluoropyrimidines.Fluoropyrimidine represents the cornerstone of many types of cancer and each year almost two million cancer patients undergo this treatment.Fluoropyrimidine-induced cardiotoxicity can be manifested in several forms,from angina pectoris to sudden death.This paper is a review of how the cardiotoxicity of fluoropyrimidines is presented,the mechanisms of its occurrence,its diagnosis,and management. | Andrada Larisa Deac Claudia Cristina Burz Ioana Corina Bocsan Anca Dana Buzoianu | 2020 | World Journal of Clinical Oncology2020，11，12： | 2 |
| 14 | Critically ill patients with cancer: A clinical perspective显示文摘Cancer patients account for 15%of all admissions to intensive care unit(ICU)and 5%will experience a critical illness resulting in ICU admission.Mortality rates have decreased during the last decades because of new anticancer therapies and advanced organ support methods.Since early critical care and organ support is associated with improved survival,timely identification of the onset of clinical signs indicating critical illness is crucial to avoid delaying.This article focused on relevant and current information on epidemiology,diagnosis,and treatment of the main clinical disorders experienced by critically ill cancer patients. | Frank Daniel Martos-Benítez Caridad de Dios Soler-Morejón Karla Ximena Lara-Ponce Versis Orama-Requejo DailéBurgos-Aragüez Hilev Larrondo-Muguercia Rahim W Lespoir | 2020 | World Journal of Clinical Oncology2020，11，10： | 1 |
| 15 | Adriamycin induces cardiac fibrosis in mice via PRMT5-mediated cardiac fibroblast activation显示文摘Long-term treatment with adriamycin(ADR)is associated with higher incidences of cumulative cardiotoxicity manifest as heart failure.ADR-induced cardiomyopathy is characterized by extensive fibrosis that is caused by cardiac fibroblast activation.To date,however,no specific treatment is available to alleviate ADR-induced cardiotoxicity.Protein arginine methyltransferase 5(PRMT5),a major enzyme responsible for methylation of arginine,regulates numerous cellular processes such as cell differentiation.In the present study we investigated the role of PRMT5 in cardiac fibrosis.Mice were administered ADR(3 mg/kg,i.p.,every 2 days)for 2 weeks.We showed that aberrant PRMT5 expression was largely co-localized withα-SMA-positive activated cardiac fibroblasts in ADR-injected mice and in ADR-treated cardiac fibroblasts in vitro.PRMT5-overexpression exacerbated,whereas PRMT5 knockdown alleviated ADR-induced cardiac fibrosis in vivo and TGF-β1-induced cardiac fibroblast activation in vitro.We demonstrated that PRMT5-overexpression enhanced methylated-Smad3 levels in vivo and in vitro.Pretreatment with a specific PRMT5 inhibitor EPZ015666(5 nM)or overexpression of a catalytically inactive mutant of PRMT5,PRMT5(E444Q),reduced PRMT5-induced methylation of Smad3,thus suppressing PRMT5-mediated cardiac fibroblast activation in vitro.Furthermore,ADR activated cardiac fibroblasts was depending on autocrine TGF-β1.Taken together,our results demonstrate that PRMT5 promotes ADR-induced cardiac fibrosis via activating cardiac fibroblasts,suggesting that it may be a potential therapeutic target of ADR-caused cardiotoxicity. | Xiao-liang Dong Bao-hui Yuan Sheng-zhou Yu He Liu Xiao-hua Pan Jia Sun Li-long Pan | 2023 | Acta Pharmacologica Sinica2023，44，3： | 1 |
| 16 | Thyme oil and thymol abrogate doxorubicin-induced nephrotoxicity and cardiotoxicity in Wistar rats via repression of oxidative stress and enhancement of antioxidant defense mechanisms显示文摘This study aimed to assess the preventive effects of thyme oil and thymol on doxorubicin(DOX)-induced renotoxicity,cardiotoxicity,and oxidative stress in Wistar rats.Thyme oil was subjected to GC-MS analysis,which indicated that thymol was the major constituent representing 33.896%.Rats intraperitoneally injected with DOX at a dose of 2 mg/kg b.w./one per week for 7 weeks were co-treated with thyme oil and its major constituent,thymol,at doses 250 and 100 mg/kg b.w./every other day,respectively,by oral gavage for the same period.Thyme oil and thymol markedly ameliorated the raised levels of serum urea,uric acid,and creatinine in DOX-administered rats.They also reduced the elevated activities of serum CK-MB and LDH.Thyme oil was more effective than thymol in decreasing the elevated serum creatinine level and serum CK-MB activity in DOX-administered rats,thereby reflecting its more potent effect on kidney and heart functions.Lipid peroxidation significantly decreased while GSH level and GST and GPx activities significantly increased in kidney and heart of DOX-administered rats treated with thyme oil and thymol.The DOX-induced perturbed kidney histological changes including congestion of glomerulus tuft,inflammatory cells infiltration,protein cast in lumina of the renal tubule,and thickening of the parietal layer of Bowman’s capsule were remarkably ameliorated as a result of treatment with thyme oil and thymol;thyme oil was more effective.In addition,DOX-induced deleterious heart histological alterations,including intramuscular infiltration of inflammatory cells,focal necrosis of cardiac myocytes,and edema,were remarkably reduced by treatment with thyme oil and thymol.Thus,it can be concluded that DOX could induce marked toxicity in kidney and heart,and the treatment with thyme oil or thymol produced potential improvement of kidney and heart function and histological integrity via repression of oxidative stress and enhancement of antioxidant defense mechanisms. | Osama M.AHMED Sanaa R.GALALY Mai RASLAN Mennah-Allah M.A.MOSTAFA | 2020 | BIOCELL2020，44，1： | 1 |
| 17 | Can short-term fasting protect against doxorubicin-induced cardiotoxicity?显示文摘Doxorubicin(Dox) is one of the most effective chemotherapeutic agents used in the treatment of several types of cancer. However the use is limited by cardiotoxicity. Despite extensive investigation into the mechanisms of toxicity and preventative strategies, Dox-induced cardiotoxicity still remains a major cause of morbidity and mortality in cancer survivors. Thus, continued research into preventative strategies is vital. Short-term fasting has proven to be cardioprotective against a variety of insults. Despite the potential, only a few studies have been conducted investigating its ability to prevent Dox-induced cardiotoxicity. However, all show proof-of-principle that short-term fasting is cardioprotective against Dox. Fasting affects a plethora of cellular processes making it difficult to discern the mechanism(s) translating fasting to cardioprotection, but may involve suppression of insulin and insulin-like growth factor-1 signaling with stimulated autophagy. It is likely that additional mechanisms also contribute. Importantly, the literature suggests that fasting may enhance the antitumor activity of Dox. Thus, fasting is a regimen that warrants further investigation as a potential strategy to prevent Dox-induced cardiotoxicity. Future research should aim to determine the optimal regimen of fasting, confirmation that this regimen does not interfere with the antitumor properties of Dox, as well as the underlying mechanisms exerting the cardioprotective effects. | Amie J Dirks-Naylor Samir A Kouzi Sendra Yang Ngan TK Tran Joseph D Bero Raean Mabolo Diep T Phan Stephanie D Whitt Heather N Taylor | 2014 | World Journal of Biological Chemistry2014，5，3： | 1 |
| 18 | Long Term Perinatal Deltamethrin Exposure Alters Electrophysiological Properties of Embryonic Ventricular Cardiomyocyte显示文摘Increased use of pyrethroids and the exposure to pyrethroids for pregnant women and children have raised the concerns over the potential effect of pyrethroids on developmental cardiotoxicity and other abnormalities.The purpose of this study was to investigate whether long tenn peri natal deltamethrin exposure altered embryonic cardiac electrophysiology in mice.Pregnant mice were administered with 0 or 3 mg/kg of deltamethrin by gavage daily from gestational day(gd)10.5 to gd 17.5.Whole cell patch-clamp technique was used in electrophysiological study,and real time RT-PCR was applied to analyze the molecular changes for the electrophysiological properties.Deltamethrin exposure resulted in increased mortality of pregnant mice and decreased viability of embryos.Moreover,deltamethrin slowed the maximum depolarization velocity(Vmax),prolonged the action potential duration(APD)and depolarized the maximuin diastolic potential(MDP)of embryonic cardiomyocytes.Additionally,perinatal deltamethrin exposure decreased the mRNA expression of Na^+channel regulatory subunit Navpl,inward rectifier K^+channel subunit Kir2.1,and delayed rectifier K^+channel subunit MERG while the L-type Ca^2+channel subunit,Cavl.2 expression was increased.On the contraiy,deltamethrin administration did not significantly alter the regulation ofβ-adrenergic or muscarinic receptor on embryonic cardiomyocytes.In conclusion,deltamethrin exposure at perinatal stage significantly alters mRNA expression of embryonic cardiac ion channels and therefore influences embryonic cardiac electrophysiological properties.This highlights the need to understand the persistent effects of pyrethroid exposure on cardiac function during embryonic development due to potential for cardiac arrhythmogenicity. | Hong-yan LUO Jacob Masika Xiu-wen Guan Li NIE Dong-hui AO Yu QI Rui SHI Jurgen Hescheler Ying ZENG | 2019 | Current Medical Science2019，39，1： | 1 |
| 19 | Midazolam in rabbits terminates dysrhythmias caused by intracerebroventricular ropivacaine显示文摘The current study was designed to investigate the mechanisms by which ropivacaine may act within the central nervous system (CNS) to produce cardiotoxicity.Eighty New Zealand rabbits were divided into four groups randomly.In Group 1,20 rabbits received intracerebroventricular (icv) saline,and then received icv ropivacaine 30 min later.In Group 2,20 rabbits received icv ropivacaine.Whenever dysrhythmias continued for more than 5 min,0.1 ml saline was administered into the left cerebral ventricle.Ten minutes later,0.1 ml midazolam was given into the left lateral ventricle.In Group 3,20 rabbits received icv ropivacaine,and once the dysrhythmias developed,the inspired isoflurane concentration was increased from 0.75% to 1.50%.In Group 4,20 animals received an intravenous (iv) phenylephrine infusion until dysrhythmias occurred.In Group 1,the rabbits did not develop dysrhythmias in response to icv saline,whereas dysrhythmias did develop in these animals after icv ropivacaine.In Group 2,icv saline had no effect on the dysrhythmias;however,icv midazolam terminated cardiac dysrhythmias.In Group 3,an increase in the concentration of the inspired isoflurane had no effect on dysrhythmias.In Group 4,icv midazolam had no effect on dysrhythmias in response to iv phenylephrine.Ropivacaine administered directly into the CNS is capable of producing cardiac dysrhythmias;midazolam terminated dysrhythmias presumably by potentiation of γ-aminobutyric acid (GABA) receptor activity.Our results suggest that ropivacaine produces some of its cardiotoxicity not only by the direct cardiotoxicity of the drug,but also by the CNS effects of ropivacaine. | Yao-min ZHU Zu-yi YUAN Hui WU Dan-dan ZHOU Gui-xia JING | 2011 | Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)2011，12，8： | 1 |
| 20 | Shengmai San for Treatment of Cardiotoxicity from Anthracyclines:A Systematic Review and Meta-Analysis显示文摘Objective:To systematically evaluate the efficacy of Shengmai San in patients with cardiotoxicity of anthracyclines.Methods:Randomized controlled trials(RCTs)were identified by searching China National Knowledge Infrastructure(CNKI),Wanfang Database,Chinese Biomedical Literature Database(CBM),Pub Med,Cochrane Library,and Embase Databases from the inceptions until December 2020.The Cochrane Handbook was used to evaluate the risk of bias in the included studies.Data analysis was conducted using Rev Man 5.3 software.Results:Totally 19 RCTs with 2,331 participants were included in this review.Results showed that in improving arrhythmia(13 RCTs,n=1,877,RR=0.37,95%CI 0.25 to 0.52,P<0.00001),the treatment group was superior to the control group.In terms of reducing left ventricular end-diastolic diameter(LVEDD,2 RCTs,n=128,MD=-0.79,95%CI-0.93 to-0.65,P<0.00001)and left ventricular end systolic diameter(LVESD,2 RCTs,n=128,MD=-0.58,95%CI-0.82 to-0.35,P<0.00001),the treatment group was also better than the control group.In reducing myocardial enzymes such as creatine kinase(CK)[(3 RCTs,n=256,SMD=-0.80,95%CI-1.16 to-0.44,P<0.0001),(2 RCTs,n=126,SMD=-0.62,95%CI-0.98 to-0.26,P=0.0007)],the treatment group was superior to the control group.Conclusion:Shengmai San has a positive effect on the treatment of cardiotoxicity from anthracyclines.However,in the future,it is still necessary to conduct high-quality RCTs to verify its efficacy. | ZHANG Xiao-nan LI Yan-yang ZHANG Yuan-hui ZHANG Wan-qin ZHU Ya-ping ZHANG Jun-ping LV Shi-chao LIU Long-tao | 2022 | Chinese Journal of Integrative Medicine2022，28，4： | 1 |
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