Effect of Tirapazamine and Mild Temperature Hyperthermia on the Recovery from Radiation-Induced Damage in Pimonidazole-Unlabeled Quiescent Tumor Cell Population

The aim in this study is to examine the effect of tirapazamine (TPZ) and mild temperature hyperthermia (MTH) on the repair of radiation-induced damage in pimonidazole-unlabeled quiescent (Q) tumor cells. Labeling of proliferating (P) cells in C57BL/6J mice bearing EL4 tumors was achieved by continuous administration of 5-bromo-2-deoxyuridine (BrdU). Tumors were irradiated with γ-rays at 1 h after the administration of pimonidazole followed by TPZ treatment or MTH. Twenty-four hours later, assessment of the responses of Q and total (= P + Q) cells were based on the frequencies of micronucleation and apoptosis using immunofluorescence staining for BrdU. The response of the pimonidazole-unlabeled tumor cell fractions was assessed by means of apoptosis frequency using immunofluorescence staining for pimonidazole. With γ-rays only, the pimonidazole-unlabeled cell fraction showed significantly enhanced radio-sensitivity compared with the whole cell fraction more remarkably in Q cells than total cells. However, a significantly greater decrease in radio-sensitivity in the pimonidazole-unlabeled than the whole cell fraction, evaluated using a delayed assay, was more clearly observed in Q cells than total cells. Post-irradiation MTH more remarkably repressed the decrease in radio-sensitivity in the Q cell than the total cells. Post-irradiation TPZ administration produced a large radio-sensitizing effect on both total and Q cells, especially on Q cells. On the other hand, in pimonidazole-unlabeled cell fractions in both total and Q cells, TPZ suppressed the reduction in sensitivity due to delayed assay much more efficiently than MTH, whereas no radio-sensitizing effect was produced. Not only through suppressing the recovery from radiation-induced damage but also through radio-sensitizing effect, post-irradiation TPZ administration is very useful for repressing the increase in the difference in radio-sensitivity due to the delayed assay not only between total and Q tumor cells but also between the pimonidazole-unlabeled and the whole cell fractions within the total and Q tumor cells.

Cardiac damage in athlete's heart: When the “supernormal” heart fails!

Intense exercise may cause heart remodeling to compensate increases in blood pressure or volume by increasing muscle mass. Cardiac changes do not involve only the left ventricle, but all heart chambers. Physiological cardiac modeling in athletes is associated with normal or enhanced cardiac function, but recent studies have documented decrements in left ventricular function during intense exercise and the release of cardiac markers of necrosis in athlete's blood of uncertain significance. Furthermore, cardiac remodeling may predispose athletes to heart disease and result in electrical remodeling, responsible for arrhythmias. Athlete's heart is a physiological condition and does not require a specific treatment. In some conditions, it is important to differentiate the physiological adaptations from pathological conditions, such as hypertrophic cardiomyopathy, arrhythmogenic dysplasia of the right ventricle, and non-compaction myocardium, for the greater risk of sudden cardiac death of these conditions. Moreover, some drugs and performance-enhancing drugs can cause structural alterations and arrhythmias, therefore, their use should be excluded.

Markers of Heart, Lung and Dorsal Aorta Damage of Mother Rats and Their Neonates Post Therapeutic Treatment with Doxorubicin, Cisplatin and 5-Flurouracil

Aim: Recently, there is an increased average of developing cancers. Though, the chemotherapeutic-treatment is unfavorable during pregnancy due to its harmful effects on developing fetuses, physicians have two ways to minimize these effects either by termination of the pregnancy or minimizing its side effects. The present work aimed to illustrate the susceptibility of cardiac, lung and dorsal aorta function to the widely applicable drugs doxorubicin and cisplatin as well as 5-flurouracil. Materials and Methods: Mother albino rats were arranged into four-groups (control, doxorubicin, cisplatin and 5-flurouracil-treated groups). Each pregnant rat received intraperitoneal administration of 0.2 mg/kg body weight at 10th and 14th day of gestation and sacrificed at parturition (two doses). At parturition, serum of mother rats used to assess troponin I, heat shock protein 70, 8-hydroxydeoxyguanosine, vascular endothelial growth factor and adhesion molecules (ICAM-1 & VCAM-1). Isoenzyme electrophoresis of alkaline and acid phosphatases, glucose-6-phosphate dehydrogenase and lactic dehydrogenase were estimated in serum, myocardium and dorsal aorta of mother rats. The myocardium and lung were processed for histopathological investigations for both mothers and their offspring. Single strand (comet assay) and double strand DNA damage were carried out in heart and dorsal aorta of mother rats. Results: The present finding revealed that there are detected alterations of myocardial markers and lung amino acid metabolism as well as disruption of myocardial isoenzymes. DNA damage of myocardium and dorsal aorta were observed. Conclusions: The authors concluded that the metabolic activity of heart and lung is highly susceptible to doxorubicin and cisplatin treatment compared to 5-flurouracil and the therapeutic doses must be degraded.

Discussion on the Prevention and Treatment of COVID-19 Causing Lung Disease and Heart Damage Based on Lei Zhongyi's Theory of Intermingled Phlegm,Blood Stasis and Toxin

Novel coronavirus infection not only damages lung function,but also causes myocardial injury,elevated myocardial enzymes and heart failure,especially for patients with basic heart diseases who develop COVID-19,the first consideration should be the protection of cardiac function.Based on the theory of intermingled phlegm,blood stasis and toxin of heart disease put forward by Master Lei Zhongyi,the dialectical treatment thinking of COVID-19 patients from the concept of damage of phlegm,blood stasis and toxin to the heart were discussed.During the diagnosis,critical stage and recovery period of COVID-19,expectorant and blood-activating agents,heat and detoxification agents can be added to promote lung and asthma,free Bizheng and remove blood stasis,calm the heart and calm the mind,and promote the recovery of cardiopulmonary functions.

Biosynthesis of fungus-based oral selenium microcarriers for radioprotection and immuno-homeostasis shaping against radiation-induced heart disease

Radiation-induced heart disease(RIHD),characterized by severe oxidative stress and immune dysregulation,is a serious condition affecting cancer patients undergoing thoracic radiation.Unfortunately,clinical interventions for RIHD are lacking.Selenium(Se)is a trace element with excellent antioxidant and immune-modulatory properties.However,its application in heart radioprotection remains challenging.Herein,we developed a novel bioactive Cordyceps militaris-based Se oral delivery system(Se@CM),which demonstrated superior radioprotection effects in vitro against X-ray-induced damage in H9C2 cells through suppressing excessive ROS generation,compared to the radioprotectant Amifostine.Moreover,Se@CM exhibited exceptional cardioprotective effects in vivo against X-ray irradiation,reducing cardiac dysfunction and myocardial fibrosis by balancing the redox equilibrium and modulating the expression of Mn-SOD and MDA.Additionally,Se@CM maintained immuno-homeostasis,as evidenced by the upregulated population of T cells and M2 macrophages through modulation of selenoprotein expression after irradiation.Together,these results highlight the remarkable antioxidant and immunity modulation properties of Se@CM and shed light on its promising application for cardiac protection against IR-induced disease.This research provides valuable insights into developing effective strategies for preventing and managing RIHD.

Advances in radiation-induced heart disease diagnosis and treatment

Over the past decades,the survival rates of patients with cancer have significantly increased owing to advancements in cancer treatment strategies.Radiotherapy has become an indispensable treatment modality for thoracic tumors.While it offers benefits in treating or even potentially curing cancer,thoracic radiotherapy exposes neighboring heart tissues to ionizing radiation,elevating the risk of radiation-induced heart disease(RIHD).Despite improvements in radiotherapy techniques that have reduced the incidence of RIHD,complete avoidance of heart radiation exposure remains a challenge.Cohort studies involving atomic bomb survivors and individuals with occupational radiation exposure,even at relatively low doses,have reported a significant increase in RIHD risks.The pathological mechanisms underlying RIHD have been extensively reviewed.At present,imaging techniques and traditional cardiac biomarkers are the primary methods to diagnose RIHD,with ongoing efforts to explore additional promising markers for predicting and monitoring RIHD.Moreover,traditional and novel therapeutic strategies are being actively explored to prevent or alleviate RIHD.Insights gained from therapeutic advancements in other organ systems or heart diseases caused by different factors can provide valuable ideas for RIHD management.This review discusses the recent advancements in the diagnosis and treatment of RIHD.

Dose-dependent Cardiac Dysfunction and Structural Damage in Rats after Shortwave Radiation

Objective To detect the effects of shortwave radiation on dose-dependent cardiac structure and function in rats after radiation and to elucidate the mechanism of shortwave radiation induced cardiac injury to identify sensitive indicators and prophylactic treatment.Methods One hundred Wistar rats were either exposed to 27 MHz continuous shortwave at a power density of 5,10,and 30 mW/cm^2 for 6 min or undergone sham exposure for the control(the rats had to be placed in the exposure system with the same schedules as the exposed animals,but with an inactive antenna).The Ca^2+,glutamic oxaloacetic transaminase(AST),creatine kinase(CK)and lactate dehydrogenase(LDH)content in the peripheral serum of the rats were detected by an automatic blood biochemical analyser.The electrocardiogram(ECG)of standard lead II was recorded by a multi-channel physiological recording and analysis system.The cardiac structure of rats was observed by light and electron microscopy.Results The results showed that the 5,10,and 30 mW/cm^2 shortwave radiation caused a significant increased in the levels of Ca2+,AST,CK,and LDH in the peripheral serum of rats.The cardiac structure was damaged by radiation and showed a disordered arrangement of myocardial fibres,the cavitation and swelling of myocardial mitochondria.These injuries were most significant 7 d after radiation and were not restored until 28 d after radiation.Conclusion Shortwave radiation of 5,10,and 30 mW/cm^2 can damage rat cardiac function,including damage to the tissue structure and ultrastructure,especially at the level of the myocardial fibres and mitochondria.Shortwave radiation at 5,10,and 30 mW/cm^2 induced damage to rat heart function and structure with a dose-effect relationship,i.e.,the greater the radiation dose was,the more significant the damage was.

Extended damage range of(Al0.3Cr0.2Fe0.2Ni0.3)3O4 high entropy oxide films induced by surface irradiation

Irradiation makes structural materials of nuclear reactors degraded and failed.However,the damage process of materials induced by irradiation is not fully elucidated,mostly because the charged particles only bombarded the surface of the materials(within a few microns).In this work,we investigated the effects of surface irradiation on the indirect irradiation region of the(Al0.3Cr0.2Fe0.2Ni0.3)3O4 high entropy oxide(HEO)films in detail by plasma surface interaction.The results show that the damage induced by surface irradiation significantly extends to the indirect irradiation region of HEO film where the helium bubbles,dislocations,phase transformation,and the nickel oxide segregation were observed.

Rheumatic valvular heart disease treated with traditional Chinese medicine:A case report

BACKGROUND Rheumatic heart disease(RHD)is an autoimmune disease that leads to irreversible valve damage and heart failure.Surgery is an effective treatment;however,it is invasive and carries risks,restricting its broad application.Therefore,it is essential to find alternative nonsurgical treatments for RHD.CASE SUMMARY A 57-year-old woman was assessed with cardiac color Doppler ultrasound,left heart function tests,and tissue Doppler imaging evaluation at Zhongshan Hospital of Fudan University.The results showed mild mitral valve stenosis with mild to moderate mitral and aortic regurgitation,confirming a diagnosis of rheumatic valve disease.After her symptoms became severe,with frequent ventricular tachycardia and supraventricular tachycardia>200 beats per minute,her physicians recommended surgery.During a 10-day preoperative waiting period,the patient asked to be treated with traditional Chinese medicine.After 1 week of this treatment,her symptoms improved significantly,including resolution of the ventricular tachycardia,and the surgery was postponed pending further follow-up.At 3-month follow-up,color Doppler ultrasound showed mild mitral valve stenosis with mild mitral and aortic regurgitation.Therefore,it was determined that no surgical treatment was required.CONCLUSION Traditional Chinese medicine treatment effectively relieves symptoms of RHD,particularly mitral valve stenosis and mitral and aortic regurgitation.

基于毒邪与络病学说探讨免疫炎症在慢性心力衰竭中作用

慢性心力衰竭(以下简称心衰),是各种心脏疾病的终末期阶段,其发病机制与免疫炎症密切相关。免疫细胞激活后,产生大量炎症因子,损伤心肌细胞,导致心肌纤维化、心室重构等病理改变。“毒损心络”是心衰发生、发展的主要病机,贯穿心衰发展的始终,以不同的形式影响心衰的发展及预后。该文通过查阅相关文献,基于毒邪与络病学说,从免疫炎症与心衰的关系及中药防治进行系统梳理,提出心衰早期,以心气虚为主,兼心气阴虚,尚未化毒、入络;心衰中期,心气亏虚为本,痰浊、瘀血、水饮留滞络脉,有化毒、入络趋势;心衰晚期,痰、瘀、水蕴结成毒,损伤心络。中药以复方治疗为主,多具有益气温阳、化瘀利水、解毒通络之功效,通过恢复M1/M2、Th1/Th2及Th17/Treg细胞之间的动态平衡,调节促炎/抗炎因子,从根本上祛除或缓解因毒邪产生的病理状态,减轻炎症,调整心之气血阴阳,达到扶正祛邪、保护心功能的作用,为临床防治心衰提供指导。

THE EXPERIMENTAL RESEARCH ON CARDIOPLEGIC SOLU-TION CONTAINING SELENIUM AND MAGNESIUM AGAINST MYOCARDIAL ISCHEMIA REPERFUSION DAMAGE

The model of this test was set up according to Langendoff isolated heart reperfusion mechanics. The experimental research was designed to observe the protective effects on ischemic andreperfuslon myocardial tissue by using ST. Thomas cardioplegic solution containing selenium andmagnesium. We conclude that using cold crystallold cardioplegic solution containing Se'+, Mg' 4 canobviously reduce ischemic and reperfusion myocardlal injury and bas an advantage of recovering myocardial runctlon after operation by observing the content or lactic dehydrogenase (LDH); creatineI,kasphoklnase CK in the coronary vessel's sinus reflux solutlonl glutatblone peroxldase (GPX); suI,eroxlde dismutase (SOD); maloydladehyde (MDA ) I Se4+ .Mg'+ .Ca'+ and cia-nging or myocardialultrastructure.

胡黄连苷Ⅱ调节HMGB1/RAGE信号通路对冠心病大鼠内皮细胞损伤的影响

目的:初步探讨胡黄连苷Ⅱ(P-Ⅱ)调节高迁移率族蛋白B1(HMGB1)/晚期糖基化终末产物受体(RAGE)信号通路对冠心病(CHD)大鼠内皮细胞损伤的影响。方法:SPF级SD大鼠随机分为control组、CHD组、P-Ⅱ低、中、高剂量组、P-Ⅱ高剂量+DEX组(P-Ⅱ高剂量+HMGB1/RAGE信号通路激活剂DEX),除control组外,采用高脂饮食联合腹腔注射垂体后叶素法建立CHD大鼠模型,灌胃或腹腔注射相应药物,1次/d,连续4周。生化分析仪分析大鼠血脂水平;ELISA检测血清血管内皮损伤标志物一氧化氮(NO)、内皮素(ET)-1、血管紧张素Ⅱ(AngⅡ)及血清和冠状动脉组织TNF-α、IL-1β、IL-6炎症因子水平;试剂盒检测大鼠冠状动脉组织活性氧(ROS)、谷胱甘肽过氧化物酶(GSH-Px)水平;HE染色观察大鼠冠状动脉组织病理损伤;TUNEL染色观察血管内皮细胞凋亡;Western blot检测冠状动脉组织中血管内皮生长因子(VEGF)、HMGB1、RAGE蛋白表达。结果:相较于control组,CHD组大鼠TC、TG、LDL-C、ET-1、AngⅡ、TNF-α、IL-1β、IL-6、ROS、内皮细胞凋亡率及HMGB1、RAGE表达显著升高,HDL-C、NO、GSH-Px及VEGF表达显著降低(P<0.05);相较于CHD组,P-Ⅱ低、中、高剂量组TC、TG、LDL-C、ET-1、AngⅡ、TNF-α、IL-1β、IL-6、ROS、内皮细胞凋亡率及HMGB1、RAGE表达显著降低,HDL-C、NO、GSH-Px及VEGF表达显著升高(P<0.05);HMGB1/RAGE信号通路激活剂DEX可减弱P-Ⅱ对CHD大鼠内皮细胞损伤的保护作用。结论:P-Ⅱ能有效减轻CHD大鼠内皮细胞损伤,其作用机制可能与抑制HMGB1/RAGE通路激活有关。

心电向量图诊断高血压早期心脏靶器官损害的临床应用及影响因素

目的探讨心电向量图(vectorcardiogram,VCG)对高血压心脏电活动异常的诊断价值,并分析早期心脏靶器官损害的影响因素。方法选取昆明市中医医院心血管病科2022年1月至2023年2月的高血压病住院患者80例,经超声心动图(ultrasound cardiogram,UCG)排外心脏结构异常。比较心电图(electrocardiogram,ECG)与VCG对异常心室除极与复极指标的检出情况。按心电向量检查结果将80例病例分为正常组(n=40)与异常组(n=40),比较2组早期心脏损害的相关影响因素指标,将差异有统计学意义的因素做二元Logistic回归分析,筛选出早期心脏损害的独立影响因素。结果VCG检出异常心室复极指标较ECG有优势(P<0.05),二者对异常除极指标的检出差异无统计学意义(P>0.05)。正常组与异常组比较,在年龄、规律服药、家族史、糖尿病、24 h平均收缩压(24 h average systolic blood pressure,24 h SBP)、白昼平均收缩压(daytime average systolic blood pressure,DSBP)、夜间平均收缩压(night average systolic blood pressure,NSBP)、血压负荷值、清晨血压、脉压差等指标上,差异有统计学意义(P<0.05)。二元Logistic回归分析显示,年龄[OR(95%CI)=0.891,0.998]、夜间平均收缩压[OR(95%CI)=1.018,2.10]、家族史[OR(95%CI)=0.029,0.499]、糖尿病[OR(95%CI)=0.042,0.916]是高血压早期心脏损害的独立影响因素。结论VCG为高血压早期心脏靶器官损害的有效检测手段。

基于“浊毒-线粒体自噬”探讨慢性肾脏病心脏损害

心脏损害是慢性肾脏病进展过程中常见并发症之一,大量研究表明线粒体自噬能干预慢性肾脏病心脏损害的病程。线粒体自噬是当今医学调控慢性肾脏病心脏损害重要靶点及研究课题。慢性肾脏病患者体内毒素代谢异常,同时心肾两脏富含线粒体,慢性肾脏病后期尿毒症毒素内积,线粒体凋亡及受损线粒体释放出的大量有害物质的过程与中医浊毒内生相似。通过从慢性肾脏病、线粒体自噬与浊毒的关系,慢性肾脏病并发心脏损害的浊毒理论,浊毒、线粒体自噬与心脏损害的联系,浊毒-线粒体自噬-慢性肾脏病并发心脏损害的形成,中医药祛浊毒理论干预线粒体自噬治疗慢性肾脏病心脏损害来论述。

皮肌炎重叠系统性硬化症心脏损害1例并临床探讨

皮肌炎以对称性近端肌无力为特征,常同时累及其他器官,多伴有血清肌酶升高及肌电图异常,合并心血管病变为其死亡危险因素之一,但临床上明显的心脏受累较为罕见,也可能是合并心脏受累的情况尚未得到重视。系统性硬化症具有复杂的发病机制和多样性的临床表现,在疾病表现上具有广泛异质性,临床表现主要以雷诺现象,皮肤受累如指端硬化、弥漫性皮肤改变,肠道动力障碍,以及心、肺、肾等脏器受损。皮肌炎重叠系统性硬化症在临床上常见,心脏损害为其重要的死亡原因之一,本文通过回顾潍坊市中医院1例皮肌炎重叠系统性硬化症导致心肌损害患者的病例资料,通过分析其临床特点,治疗转归等,并检索万方数据、知识平台PubMed、中国知网等国内外权威数据库搜索相关文献,分析、归纳其特点,从而加强临床医师对疾病的认知,提高警惕,通过早期检查、诊断以及综合治疗改善患者预后。

心中风浅析

[目的]梳理古籍文献中“心中风”的内涵、病机以及治疗,以期为临床病毒性心肌炎、癫痫等难治性疾病的治疗提供理论参佐。[方法]基于第5版《中华医典》数据库,查阅古籍文献中关于“心中风”的论述,分别从“心之义”“中之音”“风之义”三个角度辨析“心中风”的具体内涵,并概括其临床症状、病机和治疗,以期更好地指导临床。[结果]中医学之“心”乃五脏六腑之大主,不仅具有主血脉之功,尚具主藏神之能,同时部分古代医家常以“心”来代指中焦脾胃。中医学之“风”则有外风与内风之别,内风多因情志而生。故笔者基于古今文献相关论述,简要阐析“心中风”之不同内涵,其中包括血肉之心中风、神明之心中风以及其他心中风。血肉之心中风和其他心中风多由外风所致,神明之心中风可因外风或内风引起。血肉之心中风治疗以祛风药为主,佐以益气养血之药;神明之心中风则以安神药为主。[结论]血肉之心中风、神明之心中风及其他心中风分别与现代医学之病毒性心肌炎、神经系统疾病、胃肠疾病甚为相似,或可依据古籍文献为此三类疾病的临证组方提供理论依据。

蒽环类药物心脏毒副作用机制及中医药治疗研究进展

蒽环类药物是恶性肿瘤常用的化疗药物之一,但蒽环类药物引起的心脏毒性已成为恶性肿瘤治疗的最严重并发症之一,从而限制了蒽环类化疗药物的临床应用。中医药在恶性肿瘤的治疗过程中起着重要作用。中药可以预防、治疗以及减少因蒽环类药物治疗所造成的心脏毒性。在保护心肌方面,中药能够降低心肌缺血再灌注损伤、拮抗氧化应激、改善心肌重塑、调节细胞凋亡,进一步拓展了中医药治疗的应用前景。本文就近年来蒽环类药物引起心脏毒性的作用机制的研究新进展和因其治疗引起的心脏毒性方面的研究进行综述。

冠心病心绞痛患者血清内脏脂肪特异性丝氨酸蛋白酶抑制剂、不规则趋化因子、单核细胞趋化蛋白-1与心功能、心肌损伤指标相关性分析

目的:探讨冠心病(CHD)心绞痛患者血清内脏脂肪特异性丝氨酸蛋白酶抑制剂(Vaspin)、单核细胞趋化蛋白-1(MCP-1)、不规则趋化因子(Fractalkine)与心功能、心肌损伤指标的相关性。方法:选取150例CHD心绞痛患者作为观察组(不稳定型心绞痛患者64例为A组、稳定型心绞痛患者86例为B组),同期收治的164例非CHD患者为C组。比较三组血清Fractalkine、Vaspin、MCP-1水平、心功能指标及心肌损伤指标,相关性采用Pearson相关性分析。结果:A组血清Vaspin水平低于B组、C组,且与C组比较,B组更低;A组血清Fractalkine、MCP-1水平高于B组、C组,且与C组比较,B组更高(均P<0.05)。A组左心室射血分数(LVEF)、左心室短轴缩短率(FS)低于B组、C组,且与C组比较,B组更低;A组左心室舒张末期内径(LVEDD)、左室收缩末期内径(LVESD)高于B组、C组,且与C组比较,B组更高(均P<0.05)。A组各心肌损伤指标水平均高于B组、C组,且与C组比较,B组更高(均P<0.05)。Pearson相关性分析:CHD心绞痛患者血清Vaspins水平与LVEF、FS成正比;血清Vaspins水平与LVEDD、LVESD、肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、肌钙蛋白I(cTnI)、心型脂肪酸结合蛋白(H-FABP)成反比;血清Fractalkine、MCP-1与LVEF、FS成反比;血清Fractalkine、MCP-1与LVEDD、LVESD、CK、CK-MB、cTnI、H-FABP成正比(均P<0.05)。结论:随着CHD心绞痛患者病情加重,患者心功能及心肌损伤越严重,且患者血清Vaspins、Fractalkine、MCP-1与患者心功能及心肌损伤具有密切联系,临床可根据其水平变化评估病情进展情况。

虎杖苷调节Hippo/YAP信号通路对冠心病大鼠心肌损伤的影响

目的探讨虎杖苷(PD)对冠心病(CHD)大鼠心肌损伤及Hippo-Yes相关蛋白(YAP)信号通路的影响。方法构建CHD大鼠模型,将造模成功大鼠随机分为模型组(CHD组)、虎杖苷低、高剂量组(PD-L、PD-H组)、虎杖苷高剂量+Hippo/YAP信号通路激活剂PY-60组(PD-H+PY-60组),每组18只,另取18只正常大鼠作为对照组(Control组),超声心动图检测大鼠心功能。每组随机选择6只大鼠处死取心脏组织,HE染色观察大鼠心肌组织的病理形态变化,Masson染色观察大鼠心肌纤维化程度及胶原纤维化面积;TUNEL染色观察心肌组织中细胞凋亡情况;Western blot法检测B淋巴细胞瘤-2相关X蛋白(Bax)、半胱氨酸蛋白酶-3(Caspase-3)、p-YAP/YAP、具有PDZ结合模体的转录激活因子(TAZ)表达。结果CHD组较Control组心肌细胞异常,心肌纤维结构紊乱,炎性细胞浸润及组织水肿明显,蓝色胶原纤维沉积增多,心肌胶原纤维化面积占比增多,细胞凋亡率及Bax、Caspase-3、p-YAP/YAP、TAZ表达升高,左室射血分数(LVEF)、左室缩短分数(LVFS)、舒张早期运动速度/舒张晚期运动速度(Em/Am)水平降低(均P<0.05);PD-L组、PD-H组较CHD组心肌细胞形态相对正常,细胞坏死减少,炎性细胞浸润及组织水肿明显减轻,蓝色胶原纤维沉积减少,心肌胶原纤维化面积占比减少,细胞凋亡率及Bax、Caspase-3、p-YAP/YAP、TAZ表达降低,LVEF、LVFS、Em/Am水平升高(均P<0.05);PD-H+PY-60组较PD-H组心肌组织损伤加重,蓝色胶原纤维沉积增多,心肌胶原纤维化面积占比增多,细胞凋亡率及Bax、Caspase-3、p-YAP/YAP、TAZ表达升高,LVEF、LVFS、Em/Am水平降低(均P<0.05)。结论虎杖苷可改善CHD大鼠心肌损伤,其作用机制与抑制Hippo/YAP通路有关。