ETHNOPHARMACOLOGICAL RELEVANCE:Linggan Wuwei Jiangxin Decoction (LWJD), a classical formula documented in Zhang Zhongjing's Jin Gui Yao Lue, composed of multiple herbal components, is widely used for respiratory diseases associated with cold-phlegm obstructing the lungs, such as Chronic Obstructive Pulmonary Disease (COPD) and bronchial asthma, demonstrating significant clinical efficacy. However, the mechanisms underlying its therapeutic effects on these conditions remain to be elucidated. AIM OF THE STUDY:This study aims to investigate the mechanisms by which LWJD alleviates airway inflammation in COPD-like model through network pharmacology analysis and experimental validation, providing a theoretical basis for its clinical application. MATERIALS AND METHODS:Core targets of LWJD for COPD treatment were predicted using network pharmacology analysis and protein-protein interaction network prediction. Key signaling pathways of LWJD action were identified through KEGG pathway and GO enrichment analyses. A COPD model was established by cigarette smoke exposure and lipopolysaccharide (LPS) injection to simulate the disease. Inflammatory cytokine levels in bronchoalveolar lavage fluid (BALF) and serum were measured by ELISA, while inflammatory cell proportions were evaluated via routine blood tests. Pathological changes in tracheal and lung tissues were examined using hematoxylin and eosin (H&E) and Masson staining. Expression of relevant mRNAs and proteins in lung tissue was assessed by quantitative real-time reverse transcription PCR (qRT-PCR) and Western blotting. To further investigate LWJD's anti-inflammatory mechanisms, LPS-induced inflammation was modeled in BEAS-2B human bronchial epithelial cells. The regulatory effects of LWJD on the AGE-RAGE signaling pathway were evaluated by qRT-PCR and Western blotting. Immunofluorescence detected nuclear translocation of downstream NF-κB p65. Reactive oxygen species (ROS) levels in cells were quantified by flow cytometry. Adherent neutrophil counts were observed via Calcein-AM fluorescent labeling. RESULTS:Network pharmacology and pathway enrichment analysis identified core targets and key signaling pathways of LWJD for COPD. Active components in LWJD bound COPD-related targets associated with the AGE-RAGE pathway. In vivo experiments showed LWJD reduced inflammatory cytokine secretion, cell proportions, and pathological changes in COPD model mice, inhibiting the AGE-RAGE pathway to suppress responses and alleviate airway inflammation and mucus secretion. In vitro experiments showed that LWJD inhibited adhesion molecule expression, reduced nuclear translocation of NF-κB p65, lowered reactive oxygen species levels, and decreased cell adhesion. CONCLUSIONS:LWJD alleviates airway inflammation and mucus secretion in COPD by inhibiting the AGE-RAGE signaling pathway, thereby reducing NF-κB-mediated inflammatory cytokine release and inflammatory cell infiltration.

Hypertensive heart disease (HHD) arises from chronic hypertension--induced cardiac remodeling (characterized by concentric hypertrophy, fibrosis, and diastolic dysfunction) and is driven, in part, by Ang II--mediated cardiomyocyte apoptosis, oxidative stress, and fibrotic signaling. To address this, we engineered a 1-DASAATPMS@CP1@Eth nanocomposite, synthesized by conjugating compound 1 to DASA and grafting onto 3-Aminopropyltrimethoxysilane (ATPMS) to form similar to 200 nm spheres, then encapsulating CP1 (85% loading) and adsorbing ethoxysanguinarine (Eth). In Ang II-treated H9c2 cells, Eth-loaded nanoparticles (Eth-NPs) significantly preserved cell viability (CCK-8 assay) and down-regulated pro-apoptotic Bax mRNA (qPCR) compared to free Eth or blank nanoparticles. These findings indicate that the nanoparticle delivery system amplifies Eth's anti-apoptotic efficacy and offers a promising strategy for targeting cardiomyocyte apoptosis in HHD treatment.

The epithelial-mesenchymal transition (EMT) transcription factor TWIST1 plays a critical role in breast cancer progression. This study reveals that TWIST1 acetylation, which is elevated in metastatic breast cancer tissues, is regulated by a deubiquitination-acetylation crosstalk. We demonstrate that ZRANB1 binds to and deubiquitinates TWIST1, thereby increasing its protein stability. This stabilization enhances the interaction between TWIST1 and the acetyltransferase ACSS2, leading to further TWIST1 acetylation. ACSS2 overexpression reversed ZRANB1 knockdown-induced inhibition of TWIST1 acetylation. Functionally, ZRANB1 overexpression promoted breast cancer cell proliferation, invasion, migration, and EMT in vitro, as well as lung metastasis in vivo, all of which were reversed by ACSS2 knockdown. Conversely, ACSS2 knockdown suppressed TWIST1 acetylation, EMT, and metastatic capabilities. Consistently, ACSS2 overexpression rescued the inhibitory effects of ZRANB1 knockdown on breast cancer cell viability, proliferation, migration, and invasion. In summary, our findings identify a novel regulatory axis wherein ZRANB1-mediated deubiquitination facilitates ACSS2-dependent acetylation to stabilize TWIST1, thereby driving EMT and metastasis in breast cancer. The ZRANB1/ACSS2 axis presents a promising therapeutic target for combating metastasis.

BACKGROUND:Hypoparathyroidism (HypoPT) is a rare endocrine disease characterized by hypocalcemia, hyperphosphatemia, and insufficient or no parathyroid hormone (PTH) secretion. Hypoparathyroidism-induced chronic hypocalcemia may lead to cardiovascular complications, including myocardial dysfunction and arrhythmias. Interventricular septal dissecting aneurysm, a rare cardiac anomaly, typically arises following structural or ischemic heart disease. This disease can lead to ventricular septal rupture and aneurysmal cystic chamber formation, causing changes in cardiac structure and hemodynamics as well as giving rise to various heart complications. CASE PRESENTATION:No study has reported an association between hypocalcemia and cardiac masses. We encountered a case of hypoparathyroidism in a middle-aged woman who developed an interventricular septal dissecting aneurysm. Upon examination, we found that HypoPT has a profound impact on the heart. CONCLUSIONS:Hypocalcemia caused by HypoPT can result in structural changes in the heart and myocardial injury. Furthermore, there is a potential link between HypoPT and cardiac aneurysm. The development of an interventricular septal dissecting aneurysm can lead to various cardiac complications; therefore, its early diagnosis and treatment are necessary.

BACKGROUND:Pulmonary hypertension (PH) is a progressive and life-threatening disease characterized by pulmonary vascular remodeling, which involves aberrant proliferation and apoptosis resistance of the pulmonary arterial smooth muscle cells (PASMCs), resembling the hallmark characteristics of cancer. In cancer, the HMGB2 (high-mobility group box 2) protein promotes the pro-proliferative/antiapoptotic phenotype. However, the function of HMGB2 in PH remains uninvestigated. METHODS:Smooth muscle cell (SMC)-specific HMGB2 knockout or HMGB2-OE (HMGB2 overexpression) mice and HMGB2 silenced rats were used to establish hypoxia+Su5416 (HySu)-induced PH mouse and monocrotaline-induced PH rat models, respectively. The effects of HMGB2 and its underlying mechanisms were subsequently elucidated using RNA-sequencing and cellular and molecular biology analyses. Serum HMGB2 levels were measured in the controls and patients with pulmonary arterial (PA) hypertension. RESULTS:HMGB2 expression was markedly increased in the PAs of patients with PA hypertension and PH rodent models and was predominantly localized in PASMCs. SMC-specific HMGB2 deficiency or silencing attenuated PH development and pulmonary vascular remodeling in hypoxia+Su5416-induced mice and monocrotaline-treated rats. SMC-specific HMGB2 overexpression aggravated hypoxia+Su5416-induced PH. HMGB2 knockdown inhibited PASMC proliferation in vitro in response to PDGF-BB (platelet-derived growth factor-BB). In contrast, HMGB2 protein stimulation caused the hyperproliferation of PASMCs. In addition, HMGB2 promoted PASMC proliferation and the development of PH by RAGE (receptor for advanced glycation end products)/FAK (focal adhesion kinase)-mediated Hippo/YAP (yes-associated protein) signaling suppression. Serum HMGB2 levels were significantly increased in patients with PA hypertension, and they correlated with disease severity, predicting worse survival. CONCLUSIONS:Our findings indicate that targeting HMGB2 might be a novel therapeutic strategy for treating PH. Serum HMGB2 levels could serve as a novel biomarker for diagnosing PA hypertension and determining its prognosis.

Objective This study aimed to investigate the serum levels of Peptidase M20 domain containing 1 (PM20D1) in idiopathic pulmonary arterial hypertension (IPAH) patients and examine its association with lipid metabolism, echocardiography, and hemodynamic parameters.Methods This prospective observational research enrolled 103 IPAH patients from January 2018 to January 2022. Enzyme-linked immunosorbent assay (ELISA) was used to measure the serum PM20D1 levels in all patients before treatment within 24 h of admission. Demographic data, echocardiography, hemodynamic parameters and serum biomarkers were also collected.Results The IPAH patients in the deceased group had significantly elevated age, right atrial (RA), mean pulmonary arterial pressure (mPAP), mean right atrial pressure (mRAP), pulmonary capillary wedge pressure (PCWP), pulmonary vascular resistance (PVR) and significantly decreased 6 min walking distance (6MWD) and tricuspid annulus peak systolic velocity (TASPV). IPAH patients showed significant decreases in serum PM20D1, low-density lipoprotein cholesterol (LDL-C), and albumin (ALB). Additionally, PM20D1 was negatively correlated with RA, NT-proBNP and positively correlated with PVR, ALB, 6MWD, and TAPSV. Moreover, PM20D1 has the potential as a biomarker for predicting IPAH patients' prognosis. Finally, logistic regression analysis indicated that PM20D1, ALB, NT-proBNP, PVR, TASPV, RA and 6MWD were identified as risk factors for mortality in IPAH patients.Conclusion Our findings indicated that the serum levels of PM20D1 were significantly decreased in IPAH patients with poor prognosis. Moreover, PM20D1 was identified as a risk factor associated with mortality in IPAH patients.

Cardiomyopathy (CM) represents a heterogeneous group of diseases primarily affecting cardiac structure and function, with genetic and epigenetic dysregulation playing a pivotal role in its pathogenesis. Emerging evidence from the burgeoning field of epitranscriptomics has brought to light the significant impact of various RNA modifications, notably N6-methyladenosine (m6A), 5-methylcytosine (m5C), N7-methylguanosine (m7G), N1-methyladenosine (m1A), 2′-O-methylation (Nm), and 6,2′-O-dimethyladenosine (m6Am), on cardiomyocyte function and the broader processes of cardiac and vascular remodelling. These modifications have been shown to influence key pathological mechanisms including mitochondrial dysfunction, oxidative stress, cardiomyocyte apoptosis, inflammation, immune response, and myocardial fibrosis. Importantly, aberrations in the RNA methylation machinery have been observed in human CM cases and animal models, highlighting the critical role of RNA methylating enzymes and their potential as therapeutic targets or biomarkers for CM. This review underscores the necessity for a deeper understanding of RNA methylation processes in the context of CM, to illuminate novel therapeutic avenues and diagnostic tools, thereby addressing a significant gap in the current management strategies for this complex disease.

目的 研究慢性心力衰竭伴发焦虑抑郁对患者血清5-羟色胺(5-HT)、尿酸、胱抑素C和血管紧张素Ⅱ(Ang Ⅱ)水平的影响.方法 回顾性选取2020年9月至2022年9月右江民族医学院附属医院收治的120例CHF患者作为研究对象.根据汉密尔顿焦虑量表(HAMA)(大于7分为焦虑)、汉密尔顿抑郁量表(HAMD)(≥7分为抑郁)分数将患者分为焦虑抑郁组(n=42)和非焦虑抑郁组(n=78).焦虑抑郁组患者42例,非焦虑抑郁组患者78例.比较两组患者的5-HT、尿酸、胱抑素C、Ang Ⅱ、血肌酐、一般自我效能感量表(GSES)评分、纽芬兰纪念大学幸福度量表(MUN-SH)评分、并发症情况、生活质量.结果 焦虑抑郁组患者5-HT低于非焦虑抑郁组,尿酸、胱抑素C、血肌酐水平均高于非焦虑抑郁组,差异均有统计学意义(P＜0.05);两组患者Ang Ⅱ比较,差异无统计学意义(P＞0.05).焦虑抑郁组患者GSES评分、MUNSH评分均低于非焦虑抑郁组,差异均有统计学意义(P＜0.05).焦虑抑郁组并发症总发生率为42.86％,明显高于非焦虑抑郁组(16.67％),差异有统计学意义(P＜0.05).焦虑抑郁组患者躯体供能、社会功能、心理功能、物质功能、生存质量总评分均显著低于非焦虑抑郁组,差异均有统计学意义(P＜0.05).结论 慢性心力衰竭伴发焦虑抑郁患者5-HT更低,尿酸、胱抑素C、并发症总发生率更高,幸福感和生活质量更低,在慢性心力衰竭患者治疗中应注意减少焦虑抑郁的发生.

以妇产科学课程为例,对临床医学课程思政与新医科交叉重合内容进行分析,介绍妇产科学课程思政教学设计,将新医科建设的健康意识、学科融合、医者仁心等思政元素,全过程、全方位地融入课程,提升临床医学课程的教学质量.

AimsThe pathogenesis of disease progression targets for patients with heart failure after acute myocardial infarction was investigated by using plasma proteomics.MethodsThe plasma proteomes of acute myocardial infarction patients with (MI-HF) and without (MI-WHF) heart failure were compared. Each group consisted of 10 patients who were matched for age and sex. The peptides were analyzed by 2-dimensional liquid chromatography coupled to tandem mass spectrometry in a high definition mode. Parallel reaction monitoring (PRM) verified the selected target proteins.ResultsWe identified and quantified 2,589 and 2,222 proteins, respectively, and found 117 differentially expressed proteins (DEPs) (≥1.5-fold), when the MI-HF and MI-WHF groups were compared. Of these 51 and 66 were significantly up-regulated and down-regulated, respectively. The significant DEPs was subjected to protein–protein interaction network analysis which revealed a central role of the NF-κB signaling pathway in the MI-HF patients. PRM verified that MB, DIAPH1, VNN1, GOT2, SLC4A1, CRP, CKM, SOD3, F7, DLD, PGAM2, GOT1, UBA7 and HYOU1 were 14 proteins which were highly expressed in MI-HF patients.ConclusionsThese findings showed a group of proteins related to the NF-κB signaling pathway in the pathogenesis of patients with poor outcomes after experiencing MI-HF. These proteins may be useful candidate markers for the diagnosis of MI-HF as well as help to elucidate the pathophysiology of this major cause of mortality in older patients.

目的:系统评价青年急性心肌梗死发生的主要危险因素,为心肌梗死预防决策提供依据.方法:检索PubMed、Embase、Web of Science、Cochrane、Library、万方数据、中国知网(CNKI)、维普网(VIP)、中国生物医学文献数据库(CBM)等,均从建库日期检索至2022年4月的所有文献,全面收集与青年急性心肌梗死发病危险因素有关的所有病例-对照研究.由2名评价员初步筛选并独立提取资料,并评价其方法学质量.对符合要求的研究,采用RevMan 5.3和Stata 14.0统计软件对提取的相关数据进行分析.结果:最终纳入7篇病例对照研究文献,病例组1061例,对照组1627例.Meta分析结果显示吸烟[OR=2.40,95％CI(1.84,3.13)]、心血管病家族史[OR=1.97,95％CI(1.53,2.55)]、高血脂[OR=1.79,95％CI(1.52,2.12)]、高血压[OR=2.17,95％CI(1.61,2.92)]、糖尿病[OR=1.99,95％CI(1.11,3.56)]与青年急性心肌梗死发病相关.结论:吸烟、心血管病家族史、高血脂、高血压、糖尿病是目前青年急性心肌梗死发病的危险因素.

Sarcopenia is an aging syndrome characterized by decreased muscle function and skeletal muscle strength or quality. It is often accompanied by atherosclerosis (AS), which poses a great threat to the health and quality of life of the elderly. However, the relationship between sarcopenia and AS is poorly understood, so the clinical establishment of preventive measures for sarcopenia combined with AS requires further investigation. This paper aims to explore the genetic and environmental risk factors of sarcopenia complicated with AS. The clinical data of 252 non-blood-related patients with sarcopenia admitted to our hospital from May 2016 to May 2020 were retrospectively analyzed and allocated to AS and non-AS groups basing on whether they had concurrent AS. Univariate analysis found statistically significant ( P <0.05) differences between the two groups’ vitamin D receptor (VDR) Fok I loci genotypes and alleles, Xba I XX loci genotypes and alleles, ages, family history of AS, merge inflammation, growth hormone (GH) levels, insulin-like growth factor 1 (IGF-1) levels, testosterone levels, estrogen levels, insulin resistance (IR), vitamin D deficiency, and bone density. A multivariable logistic regression analysis showed VDR Fok I loci genotypes and alleles, Xba I XX loci genotypes and alleles, merge inflammation, GH levels, IGF-1 levels, low testosterone levels, low estrogen levels, and vitamin D deficiency were independent risk factors of sarcopenia combined with AS. Therefore, corresponding preventive measures should be taken for the above risk factors in clinical practice to reduce the incidence of sarcopenia combined with AS.

Abstract Background: In recent years, the FLNC gene has been shown to participate in dilated cardiomyopathy (DCM) through different mechanisms, and its variants are a common cause of hereditary DCM. This study aimed to systematically evaluate multiple FLNC effect mechanisms in DCM and to expand the spectrum of FLNC gene variations. Methods:Based on five microarray expression profile datasets downloaded from the Gene Expression Omnibus (GEO) database, comprising DCM tissue and healthy control groups, the difference in FLNC gene expression levels between the two groups was evaluated. Subsequently, differentially expressed genes (DEGs) among 81 DCM tissues were identified based on FLNC grouping, and gene ontology, Kyoto Encyclopedia of Genes and Genomes enrichment analysis, correlation analysis, and protein–protein interaction (PPI) network construction were conducted for DEGs. Based on single-sample Gene Set Enrichment Analysis method, we then evaluated differences in immune infiltration levels between the two groups using ''student 's'' and the correlation between FLNC gene expression.and the immune cells we using '' Spearman's correlation '' methods. Then, we constructed a ce-RNA network of FLNC based on several databases.Finally,100 blood samples from DCM and non-DCM individuals from the Guangxi Zhuang population in China were selected for FLNC gene sequencing, case-specific newly discovered or rare FLNC gene mutation sites were screened, and the clinical information of patients with FLNC gene mutations and their families were collected for Sanger sequencing verification. Results: FLNC expression was significantly higher in the DCM group than in the control group. After grouping 81 DCM tissues according to median FLNC expression levels, 54 DEGs were identified. The enrichment analysis shows that downregulated DEGs were more associated with inflammation and immunity, while upregulated DEGs involved actin and mitogen-activated protein kinase signaling pathways. The correlation analysis of DEGs and the PPI network identified genes associated with FLNC. According to the immune infiltration analysis, the DCM group was more associated with immunity, and the infiltrating plasma cells had a strong correlation with the FLNC gene; we identified eight miRNAs and 29 lncRNAs that bind to the FLNC gene. The final gene sequencing results show that a total of eight FLNC-specific missense mutations were detected, among which FLNCT407N and FLNCR437L are rare mutations. Additionally, the mutation frequency and minimum allele frequencies determined by sequence comparison were higher than those of databases such as the 1,000Genomes database, and all were predicted to be harmful mutations by SIFT, PolyPhen-2, and Mutation Assessor software. FLNCR437L, FLNCT834M, FLNCG1264S, FLNCR1567Q, and FLNCL2538F mutations are highly conserved among different species and were verified as heterozygous mutations by Sanger sequencing, while FLNCV452M may be the pathogenic site of DCM. Conclusion: The data analysis of myocardial tissue samples and the mutation analysis of DCM serum samples provides a rich perspective for exploring the biological functions, molecular mechanisms, immune cell correlations, ceRNA networks, and pathogenic gene mutation sites connected to FLNC in DCM.

目的 基于动脉粥样硬化(AS)家兔模型研究黑血藤在AS及肌少症预防中的药效及代谢组学,为深入研究、开发和利用黑血藤提供科学依据.方法 将健康家兔分为正常组、模型组、血脂康组和黑血藤组,正常组给予基础饲料,其它组给予高脂饲料饲喂,血脂康组和黑血藤组再分别给予血脂康生药0.36 g/(kg·d)和黑血藤提取物0.29 g/(kg· d)灌胃处理.分析AS模型家兔血清中脂质组成、超氧化物歧化酶(SOD)含量、血液流变学参数变化及主动脉弓和比目鱼肌的组织病理形态,评价黑血藤提取物预防AS及肌少症的药效;利用超高效液相色谱-四级杆飞行时间质谱(UPLC-Q-TOF-MS)研究家兔血清代谢组学,探讨黑血藤预防AS及肌少症的代谢机制.结果 黑血藤具有较好的降低血脂、改善血液流变学、抑制脂质在血管内皮沉积和增强比目鱼肌横截面积等与预防AS及肌少症相关的药效,其在AS家兔模型中预防AS的药效不及血脂康但预防肌少症的药效优于血脂康.与正常组比较,从AS模型家兔血清中鉴别出37个差异代谢物,黑血藤对其中25个差异代谢物有一定程度的回调作用;在与黑血藤药效密切相关的代谢通路中,组氨酸及精氨酸-脯氨酸代谢具有重要意义,L-谷氨酰胺和L-丙氨酸在差异代谢物关系网络及差异代谢物-通路关系网络中关联作用广泛.结论 黑血藤具有预防AS及肌少症的药效,开发其相关药物用于预防肥胖引起的AS及肌少症具有广泛的应用前景;其代谢机制与组氨酸及精氨酸-脯氨酸代谢相关,L-谷氨酰胺和L-丙氨酸可能为黑血藤药效的代谢标志物之一.

Cardiovascular disease (CVD) is the most fatal disease that causes sudden death, and inflammation contributes substantially to its occurrence and progression. The prevalence of CVD increases as the population ages, and the pathophysiology is complex. Anti-inflammatory and immunological modulation are the potential methods for CVD prevention and treatment. High-Mobility Group (HMG) chromosomal proteins are one of the most abundant nuclear nonhistone proteins which act as inflammatory mediators in DNA replication, transcription, and repair by producing cytokines and serving as damage-associated molecular patterns in inflammatory responses. The most common and well-studied HMG proteins are those with an HMGB domain, which participate in a variety of biological processes. HMGB1 and HMGB2 were the first members of the HMGB family to be identified and are present in all investigated eukaryotes. Our review is primarily concerned with the involvement of HMGB1 and HMGB2 in CVD. The purpose of this review is to provide a theoretical framework for diagnosing and treating CVD by discussing the structure and function of HMGB1 and HMGB2.

目的 为促进护理专业学生在健康中国建设中发挥作用,培养适应社会需求的护理应用型创新人才.方法 针对护理专业人才培养方案创新能力培养不突出、教学方法和教学手段单一、重理论学习轻实践锻炼、创新的文化氛围相对匮乏等问题,从教育观念、课程体系、实验平台、成长环境和创新能力等方面,围绕医工理文多学科融合教育进行探索.结果 提升了学生解决实际临床问题、实践操作和创新的能力,培养了学生护理人文观念和综合职业素养.结论 健康中国战略下多学科交叉融合的护理应用型创新人才培养模式将实践课与研究课题有机融合,有效地提升了护生和教师的实践创新能力,为健康中国战略目标的实现奠定了基础.

To observe the effect of compound lidocaine cream on oropharyngeal flora under general anesthesia, the front-end tracheal tube or laryngeal mask was coated with 410 cases under general anesthesia were chosen as endotracheal intubation group (T) and Laryngeal mask group (L) from Jan, 2022 to June, 2022. Both were separately grouped into blank control (M), liquid paraffin oil (P) and Compound lidocaine cream (C) . Based on the grouping, patients’ throat swab samples were collected for bacterial culture through tracheal catheter. Oral normal flora and pathogenic bacteria from M and P were compared and P >0.05 was considered statistically non-significant. By comparison of C, T and L group, their oral normal flora and pathogenic bacteria were obviously restrained. In conclusion, compound lidocaine cream was coated on tracheal tube or laryngeal mask for patients under general anesthesia. This method will be helpful to improve oral problems from pathogenic bacteria and also to inhibit oral normal flora.

Aluminum exposure can mediate either acute toxicity or chronic toxicity. Aluminum exerts toxic effects on the cardiovascular system, but there are few studies on its related mechanisms. In this study, we investigated the molecular mechanism of aluminum-induced oxidative damage and apoptosis in rat cardiomyocytes. Thirty-two male Wistar rats were randomly divided into four groups, including the control group (GC), low-dose group of aluminum exposure (GL), medium-dose group (GM), and high-dose group (GH), with eight rats in each group. The GL, GM, and GH groups were given 5, 10, and 20 mg/(kg·d) of AlCl3 solution by intraperitoneal injection, and the GC group received intraperitoneal injection of the same volume of normal saline (2 ml/rat/day), 5 times a week for 28 days. At the end of the experiment, the levels of aluminum, malondialdehyde (MDA), plasma lactate dehydrogenase (LDH), creatine kinase (CK), creatine kinase isoenzyme (CKMB), and alpha-hydroxybutyrate dehydrogenase (HBDH) were measured. The pathological changes of myocardium were observed by H&E staining. The apoptosis of cardiomyocytes was detected by TUNEL staining, and the expression of apoptosis-related proteins was determined by western blot. The results showed that the levels of CKMB and HBDH in the GM and GH groups were significantly higher than those in the GC group (P < 0.05). The content of aluminum in the myocardium and serum of the aluminum exposure groups was significantly higher than that of the GC group (P < 0.05). The level of MDA in the GM and GH groups was significantly higher than that in the GC group (P < 0.05). The pathological results showed that vacuolated and hypertrophied cardiomyocytes were found in aluminum exposure groups, especially in the GM and GH groups. The TUNEL staining showed that the apoptosis rate of the aluminum exposure groups was considerably higher than that of the GC group (P < 0.05). Western blot showed that the expression of Bcl-2, an anti-apoptotic protein, in cardiomyocytes of aluminum exposure groups was lower than that of the GC group (P < 0.05), while the levels of Bax and caspase-3 in the cardiomyocytes of the GM and GH groups were higher than those of the GC group (P < 0.05). The experimental results showed that aluminum could accumulate in myocardial tissues and cause damage to cardiomyocytes. It could induce oxidative stress damage by increasing the content of MDA in cardiomyocytes and trigger cardiomyocyte apoptosis by activating the pro-apoptotic proteins caspase-3 and Bax and reducing the anti-apoptotic protein Bcl-2.

目的 探讨中药龙血竭总黄酮(sanguis draconis flavones,SDF)对心肌缺血再灌注损伤(myocardial ischemia reperfusion injury,MIRI)大鼠的可能保护机制.方法 取健康成年雄性SD大鼠24只,体质量(250±20)g,按照随机数字表法分为4组:正常组(Control组)、假手术组(Sham组)、缺血/再灌注组(I/R组)、龙血竭总黄酮+缺血/再灌注组(SDF组),每组6只.I/R组和SDF组大鼠建立心肌缺血/再灌注(ischemia/reperfusion,I/R)损伤模型,即结扎冠状动脉左前降支(left anterior descending,LAD)30 min,再灌注120 min.Sham组行与I/R组相同操作,但只穿线不结扎LAD.采用实时监测心电图判断大鼠心肌I/R损伤模型构建成功与否.取各组大鼠腹主动脉血检测心肌损伤标志物CK-MB及LDH含量;HE染色法观察各组大鼠心肌组织病理学改变;TTC染色法检测各组大鼠心肌梗死面积;TUNEL染色检测各组大鼠心肌组织TUNEL阳性细胞率;采用RT-qPCR检测各组大鼠心肌组织焦亡相关分子caspase-3、GS-DME及IL-1β的mRNA表达水平.结果 Control组、Sham组在各信号通路分子表达量间均无统计学差异(P>0.05);与Control组、Sham组相比,I/R组大鼠心肌组织损伤明显,可见较多炎症细胞渗出,心肌梗死面积明显增大(P<0.01),心肌组织TUNEL阳性细胞率明显升高(P<0.01),心肌组织caspase-3、GSDME及IL-1βmRNA表达水平明显升高(P<0.01);与I/R组相比,SDF组大鼠心肌组织损伤减轻,炎症细胞渗出减少,心肌梗死面积明显减小(P<0.01),心肌组织TUNEL阳性细胞率明显降低(P<0.01),心肌组织caspase-3、GSDME及IL-1βmRNA表达水平降低(P<0.05).结论 龙血竭总黄酮对心肌缺血再灌注损伤大鼠心肌具有保护作用,可能与抑制caspase-3/GSDME信号通路激活有关.

目的 探讨广西壮族冠心病(CHD)患者的TLR4蛋白表达水平及其rs4986790A/G、rs4986791C/T位点的多态性.方法 选取2016年1月至2018年1月在我院行冠状动脉造影(CAG)检查被确诊为CHD的壮族患者245例为CHD组,选取同期在我院住院治疗的245例非CHD患者为对照组.采用酶联免疫吸附法(ELISA)检测两组患者的血清TLR4蛋白表达水平;采用SNaPshot测序技术检测两组患者外周血TLR4基因rs4986790A/G、rs4986791C/T位点的基因型及等位基因.分析TLR4蛋白表达水平及其rs4986790A/G、rs4986791C/T位点的多态性与壮族人群CHD发病的相关性.结果 CHD组患者的外周血TLR4蛋白表达水平高于对照组,差异有统计学意义(P＜0.05).CHD组患者的TLR4基因rs4986790A/G、rs4986791C/T位点的等位基因及基因型频率分布与对照组患者比较,差异无统计学意义(P＞0.05).结论 外周血TLR4蛋白表达水平与广西壮族人群CHD的发生存在关联,但TLR4基因rs4986790A/G、rs4986791C/T位点的多态性可能与壮族人群CHD冠心病发病无明显的相关性.