目的 探讨非编码长链 RNA ANRIL（lncRNA-ANRIL）通过调控miR‐181b 介导磷酸酶及张力蛋白同源物基因（PTEN）对冠状动脉粥样硬化性心脏病（冠心病）心肌损伤影响的机制。方法 纳入2023年10月—2024年6月广州市第一人民医院30例确诊为冠心病的患者为观察组, 另选择同期本院体检中心30名健康者为对照组,检测两组研究者血压指标、血脂指标以及血清 lncRNA-ANRIL、miR-181b、PTEN水平, 并比较检测结果。结果 两组的性别、年龄、BMI、吸烟、高血压一般资料对比差异无统计学意义（P>0.05）; 观察组收缩压、舒张压水平以及总胆固醇、甘油三酯、低密度脂蛋白胆固醇水平均高于对照组,而高密度脂蛋白胆固醇则低于对照组（P<0.05）; 观察组血清 lncRNA ANRIL Exon 1-2、lncRNA ANRIL Exon 17-18相对表达水平以及PTEN水平低于对照组（t=12.623、7.741、8.231, P=0.001）, 而miR-181b水平则高于对照组（t=37.250, P=0.001）。结论 相较于正常人群, 冠心病患者血清lncRNA-ANRIL和PTEN水平明显降低,而miR-181b水平升高,提示lncRNA-ANRIL可通过调控miR-181b来调节PTEN的表达, 从而影响冠心病心肌损伤的过程。
Objective To explore the mechanism of competitive binding of non coding long stranded RNA ANRIL（lncRNA-ANRIL）to miR-181b to mediate phosphatase and tensin homolog gene（PTEN）on myocardial injury in coronary heart disease．Methods Thirty patients diagnosed with coronary heart disease in our hospital from October 2023 to June 2024 were included as the observation group,and another 30 individuals from physical examination center during the same period were selected as the control group．Blood pressure indicators,blood lipid indicators, and serum levels of lncRNA-ANRIL, miR-181b, and PTEN were measured in the two groups of patients, and the test results were compared．Results There was no significant difference between the two groups in terms of gender, age, BMI, smoking and hypertension（P>0.05）．The levels of systolic blood pressure（SBP）, diastolic blood pressure（DBP）, total cholesterol（TC）, triglycerides（TG）, and low-density lipoprotein cholesterol（LDL-C） in the observation group were higher than those in the control group,while high-density lipoprotein cholesterol（HDL-C） was lower than that in the control group（P<0.05）．The relative expression levels of lncRNA-ANRIL Exon 1-2, Exon 17-18, and PTEN levels in the observation group were lower than those in the control group（t=12.623, 7.741, 8.231, P=0.001）, while the level of miR-181b was higher than that in the control group（t=37.250, P=0.001）．Conclusions Compared with healthy individuals, serum levels of lncRNA-ANRIL and PTEN are significantly reduced in patients with coronary heart disease, while miR-181b levels are elevated, indicating that lncRNA ANRIL can regulate PTEN expression by miR-181b, thereby affecting the process of myocardial injury in coronary heart disease．
脓毒症当前仍然是全球范围内重要的医疗卫生问题,其对世界公共卫生及患者安全带来重大威胁。脓毒症是指宿主对感染反应失调引起的危及生命的器官功能障碍, 其发病率和病死率均极高,是临床重症医学中的重大挑战。在脓毒症病情的进展过程中, 可出现组织灌注不足、血流动力学不稳定等变化, 从而导致多器官功能受损,而心脏是常见的被累及的重要靶器官之一, 这种由脓毒症所导致的不同程度的心肌损伤, 被称为“脓毒性心肌病”, 其发生和发展机制复杂多样, 涉及循环心肌抑制因素、心肌自身因素及自主神经失调等多个方面。文章综述了脓毒症患者发生心肌损伤的高危因素, 以期为临床治疗和预防提供参考。
Sepsis currently remains an important global healthcare issue, and a major threat to world public health and patient safety．Sepsis is a life-threatening organ dysfunction caused by dysregulation of the host response to infection, with extremely high morbidity and mortality,which is a major challenge in clinical critical care medicine．During the progression of sepsis, changes such as inadequate tissue perfusion and haemodynamic instability may occur, leading to impairment of multiple organ functions, while the heart is one of the commonly involved vital target organs, and the varying degree of myocardial damage caused by sepsis is known as “septic cardiomyopathy”．The mechanisms of its occurrence and development are complex and diverse, involving circulating myocardial inhibitory factors, myocardial auto-factors, and autonomic dysregulation．In this paper, we review the high-risk factors for myocardial injury in septic patients, providing a reference for clinical treatment and prevention.
目的 观察超声心动图(UCG)+心肌损伤标志物水平检测在急性心肌梗死(AMI)患者诊断中的应用价值。方法 选取2020年6月—2021年9月我院收治的74例AMI患者为观察组,另选取同期65例疑似AMI患者为对照组,2组均进行UCG检测,并对比入院后0~2 h、2~12 h、12~24 h心肌损伤标志物[肌酸激酶同工酶(CK-MB)、氨基末端脑钠肽前体(NT-proBNP)、肌钙蛋白(cTnI)、心脏型脂肪酸结合蛋白(H-FABP)]水平,分析心肌损伤标志物与AMI病情程度的关联性及UCG+心肌损伤标志物水平检测对AMI诊断的应用价值。结果 UCG检查结果显示观察组阳性率86.79%高于对照组9.23%(P＜0.001);对照组入院后各时间段CK-MB、NT-proBNP、cTnI、H-FABP水平差异无统计学意义(P＞0.05)观察组入院后各时间段CK-MB、NT-proBNP、cTnI、H-FABP水平均高于对照组(P＜0.05);Spearman相关分析可知,血清CK-MB、NT-proBNP、cTnI、H-FABP水平与AMI患者病情程度呈正相关(r1=0.648,r2=0.692,r3=0.704,r4=0.683,P＜0.05);受试者工作特征曲线(ROC)曲线分析显示,UCG+血清CK-MB、NT-proBNP、cTnI、H-FABP联合检测对AMI患者的诊断敏感度(85.14%)、特异度(100.00%)较高(P＜0.05)。结论 UCG+心肌损伤标志物水平检测应用于AMI患者有利于提高诊断敏感度、特异度,诊断价值较高。
目的 探讨应用超声心动图评价肺动脉高压(PAH)致心肌损伤的临床价值及氧化应激损伤的相关性。方法 12周龄SD大鼠48只。随机均分为4组:空白对照组、NaCl对照组、PAH 2周组及PAH 4周组。建模后,采用超声检测相关参数。HE及Masson染色观察右心室的心肌细胞及胶原纤维分布情况,测定超氧化物歧化酶(SOD)活力,还原型谷胱甘肽(GSH)和丙二醛(MDA)水平,并评价其与超声参数的相关性。结果 PAH组大鼠超声相关参数均变化明显,且逐渐加重。HE及Masson染色显示心肌细胞增大,心肌间隙中的胶原纤维明显增多,且4周组较明显。PAH组大鼠心肌组织中的SOD活力及GSH水平较低,而MDA水平较高,有变化趋势,且与超声参数有显著相关性,差异均有统计学意义(P<0.05)。结论 PAH导致大鼠右心室心肌组织结构改变,同时引起氧化应激相关指标的变化。
Objective To explore the clinical value of echocardiographic evaluation of myocardial injury caused by pulmonary hypertension (PAH) and the correlation of oxidative stress injury. Methods Forty-eight 12-week-old SD rats were collected. They were randomly divided into 4 groups: blank control group, NaCl control group, PAH 2-week group and PAH 4-week group. After modeling, ultrasound was used to detect relevant parameters. HE and Masson staining were used to observe the distribution of myocardial cells and collagen fibers in the right ventricle. Superoxide dismutase (SOD) activity, reduced glutathione (GSH) and malondialdehyde (MDA) levels were measured, and their correlations with ultrasound parameters were evaluated. Results The ultrasound-related parameters of rats in the PAH group changed significantly and gradually increased.HE and Masson staining showed that cardiac myocytes were enlarged and collagen fibers in myocardial interstices were increased, and it was more obvious in the 4-week group.In the PAH group, the SOD activity and GSH levels were lower, while the MDA levels were higher, and there was a trend of change, and there was a significant correlation with ultrasound parameters. The difference was statistically significant (P<0.05). Conclusion PAH causes changes in the myocardial tissue structure of the rat right ventricle, as well as changes in oxidative stress-related indicators.
目的 探讨血浆脑利钠肽前体(proBNP)和心肌损伤标志物(CK-MB和cTnI)联合检测对老年脓毒症患者心肌损伤及预后评估的临床意义。方法 选择60例老年脓毒症患者按病情严重程度分为一般脓毒症组和严重脓毒症组,另选取同期在我院行健康体检的同龄人30例作为对照组。比较三组和不同预后患者血浆proBNP、cTNI、CK-MB水平及急性生理和慢性健康状态评分Ⅱ(APACHE Ⅱ) ,并对各指标进行相关性分析。结果 脓毒症患者血浆proBNP、cTnI水平高于对照组,且严重脓毒症组APACHEⅡ评分高于一般脓毒症组(均P＜0. 05);死亡组患者其血浆中的proBNP,cTNI和CK-MB水平及APACHE Ⅱ评分均高于存活组患者(均P＜0.05),差异有统计学意义;严重脓毒症组患者血浆proBNP 水平与cTnI及CK-MB水平呈正相关性(P＜0.05); 血浆proBNP水平、cTnI水平、CK-MB水平分别与APACHEⅡ评分呈正相关性(P＜0.05)。结论 血浆proBNP 及cTnⅠ水平可有效反映老年脓毒症患者心肌受损程度,早期血浆proBNP、cTnI、CK-MB水平联合检测对老年脓毒症患者预后判断可能有重要临床意义。
Objective To study the clinical significance of cardiac injury biomarkers(CK-MB and cTnI) and pro-brain natriuretic peptide(proBNP) joint detection for prognosis value in Elderly sepsis. Methods Sixty elderly patients with sepsis were selected. According to the severity of disease divided into general and severe sepsis group.Meanwhile, 30 healthy volunteers as a control group. Comparative study of plasma proBNP, cTnI, CK-MB levels and acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ) in three groups;and the correlation analysis of the indicators. Results Compared with control group, the plasma levels of proBNP and cTnI were significantly higher in patients with sepsis; And the APACHEⅡ score in the severe sepsis group was significantly higher than the general sepsis group (P<0. 05). The plasma proBNP, cTnI, CK-MB level and APACHE Ⅱ scores in death group were significantly higher than the survival group (P<0. 05). The proBNP plasma levels, cTnⅠ and CK-MB levels in severe sepsis patients were positively correlated (P<0. 05); They were positively correlated between ProBNP level, cTnⅠ level and the APACHEⅡ score(P<0. 05). Conclusions ProBNP plasma levels and cTnⅠ can effectively reflect the extent of the cardiac damage in elderly sepsis; Early plasma proBNP level, cTnI and CK-MB combined detection of elderly sepsis may have important clinical significance.
目的 探讨抗增殖蛋白2（PHB2）脓毒症心肌损伤线粒体功能的调控机制。方法 体外培养大鼠心肌细胞株（H9C2）,分为对照组、脂多糖（LPS）组、LPS+PHB2 siRNA（si-PHB2）组。检测氧化应激指标细胞内丙二醛（MDA）水平、荧光探针检测细胞内活性氧（ROS）水平;线粒体指标：三磷酸腺苷（ATP）水平、线粒体膜电位、线粒体电镜、线粒体半定量评分;免疫印迹法检测PHB2、PTEN诱导激酶1（PTNKI）、帕金蛋白（Parkin）、线粒体转录因子（TFAM）的表达。结果 LPS刺激后MDA水平和ROS水平升高、ATP水平低,LPS+si-PHB2组MDA（6.21±0.39 vs 3.59±0.33, P<0.05）、细胞内的ROS（15 131.37±88.72 vs 8 628.67±71.95, P<0.05）的水平较LPS组升高,ATP（3.46±0.34 vs 4.52±0.25, P<0.05）和线粒体膜电位水平（0.33±0.04 vs 0.55±0.09, P<0.05）进一步降低;电镜观察显示与正常组相比,LPS组、LPS+si-PHB2组出现不同程度线粒体损伤,线粒体损伤半定量评分显示LPS+si-PHB2组的损伤较LPS组更为明显（1.42±0.10 vs 0.81±0.04, P<0.05）; 免疫印迹法结果显示LPS处理后PHB2、PINK1、Parkin 表达上调,TFAM表达下调,LPS+si-PHB2组的线粒体自噬相关蛋白PINK1（1.33±0.06 vs 1.79±0.21, P<0.05）、Parkin（1.43±0.08 vs 1.86±0.09, P<0.05）和线粒体生物发生关键蛋白TFAM（0.29±0.01 vs 0.74±0.06, P<0.05）表达均较LPS组降低。结论 LPS可促进大鼠心肌细胞PHB2表达,si-PHB2干扰后线粒体自噬蛋白和生物发生蛋白表达抑制,心肌细胞氧化应激损害和线粒体功能障碍加重,提示PHB2表达上调可能恢复线粒体稳态改善脓毒症心肌损伤的线粒体功能。
Objective To explore the regulatory mechanism of septic myocardial injury by prohibitin 2（PHB2）. Methods Rat myocardial cell lines（H9C2）were cultured in vitro and divided into control group,LPS group,LPS + PHB2 siRNA（si-PHB2） group. The indicators for detecting oxidative stress include the levels of intracellular malondialdehyde（MDA）and reactive oxygen species（ROS）. The indicators for mitochondrial detection include adenosine triphosphate（ATP）levels,mitochondrial membrane potential,mitochondrial electron microscopy,and semi-quantitative mitochondrial scoring. Western blotting was used to detect the expression of PHB2,PTEN induced putative kinase（PINK1）,Parkin,mitochondrial transcription factor A（TFAM）. Results After LPS stimulation,MDA level and intracellular ROS level increased,ATP level decreased. Compared with LPS group,MDA（6. 21±0. 39 vs 3. 59±0. 33, P<0. 05）level and intracellular ROS level（15 131. 37±88. 72 vs 8 628. 67±71. 95, P<0. 05）in LPS + si-PHB2 group increased significantly,while ATP（3. 46±0. 34 vs 4. 52±0. 25, P<0. 05）and MMP（0. 33±0. 04 vs 0. 55±0. 09, P<0. 05）level further decreased. Compared with the normal group,the structure of mitochondria in LPS group and LPS + si-PHB2 group was damaged in different degree. The semi-quantitative score of mitochondrial damage showed that the damage in LPS + si-PHB2 group was more obvious than that in LPS group（1. 42±0. 10 vs 0. 81±0. 04, P<0. 05）. Western blotting showed that the expression of PHB2,PINK1 and Parkin were up-regulated and the expression of TFAM was down-regulated after LPS treatment,mitohagy-related proteins PINK1（1. 33±0. 06 vs 1. 79±0. 21, P<0. 05）,Parkin（1. 43±0. 08 vs 1. 86±0. 09, P<0. 05）and mitochondrial biogenetic protein TFAM（0. 29±0. 01 vs 0. 74±0. 06, P<0. 05）in LPS+si-PHB2 group were lower than those in LPS group. Conclusions LPS can promote the expression of PHB2 in rat cardiomyocytes. After interfering with PHB2 expression,we found that mitochondrial autophagy and biogenesis are inhibited,and mitochondrial dysfunction,oxidative stress exacerbated,suggesting that the up-regulation of PHB2 expression may restore mitochondrial homeostasis and improve mitochondrial function in septic myocardial injury.
