[An early warning model for sepsis complicated with acute respiratory distress syndrome based on synthetic minority oversampling technique algorithm].

OBJECTIVE: To explore the independent risk factors of acute respiratory distress syndrome (ARDS) in patients with sepsis, establish an early warning model, and verify the predictive value of the model based on synthetic minority oversampling technique (SMOTE) algorithm. METHODS: A retrospective case-control study was conducted. 566 patients with sepsis who were admitted to Jinan People's Hospital from October 2016 to October 2022 were enrolled. General information, underlying diseases, infection sites, initial cause, severity scores, blood and arterial blood gas analysis indicators at admission, treatment measures, complications, and prognosis indicators of patients were collected. The patients were grouped according to whether ARDS occurred during hospitalization, and the clinical data between the two groups were observed and compared. Univariate and binary multivariate Logistic regression analysis were used to select the independent risk factors of ARDS during hospitalization in septic patients, and regression equation was established to construct the early warning model. Simultaneously, the dataset was improved using the SMOTE algorithm to build an enhanced warning model. Receiver operator characteristic curve (ROC curve) was drawn to validate the prediction efficiency of the model. RESULTS: 566 patients with sepsis were included in the final analysis, of which 163 developed ARDS during hospitalization and 403 did not. Univariate analysis showed that there were statistically significant differences in age, body mass index (BMI), malignant tumor, blood transfusion history, pancreas and peripancreatic infection, gastrointestinal tract infection, pulmonary infection as the initial etiology, acute physiology and chronic health evaluation II (APACHE II) score, sequential organ failure assessment (SOFA) score, albumin (Alb), blood urea nitrogen (BUN), mechanical ventilation therapy, septic shock and length of intensive care unit (ICU) stay between the two groups. Binary multivariate Logistic regression analysis showed that age [odds ratio (OR) = 3.449, 95% confidence interval (95%CI) was 2.197-5.414, P = 0.000], pulmonary infection as the initial etiology (OR = 2.309, 95%CI was 1.427-3.737, P = 0.001), pancreas and peripancreatic infection (OR = 1.937, 95%CI was 1.236-3.035, P = 0.004), septic shock (OR = 3.381, 95%CI was 1.890-6.047, P = 0.000), SOFA score (OR = 9.311, 95%CI was 5.831-14.867, P = 0.000) were independent influencing factors of ARDS during hospitalization in septic patients. An early warning model was established based on the above risk factors: P1 = -4.558+1.238×age+0.837×pulmonary infection as the initial etiology+0.661×pancreas and peripancreatic infection+1.218×septic shock+2.231×SOFA score. ROC curve analysis showed that the area under the ROC curve (AUC) of the model for ARDS during hospitalization in septic patients was 0.882 (95%CI was 0.851-0.914) with sensitivity of 79.8% and specificity of 83.4%. The dataset was improved based on the SMOTE algorithm, and the early warning model was rebuilt: P2 = -3.279+1.288×age+0.763×pulmonary infection as the initial etiology+0.635×pancreas and peripancreatic infection+1.068×septic shock+2.201×SOFA score. ROC curve analysis showed that the AUC of the model for ARDS during hospitalization in septic patients was 0.890 (95%CI was 0.867-0.913) with sensitivity of 85.3% and specificity of 79.1%. This result further confirmed that the early warning model constructed by the independent risk factors mentioned above had high predictive performance. CONCLUSIONS: Risk factors for the occurrence of ARDS during hospitalization in patients with sepsis include age, pulmonary infection as the initial etiology, pancreatic and peripancreatic infection, septic shock, and SOFA score. Clinically, the probability of ARDS in patients with sepsis can be assessed based on the warning model established using these risk factors, allowing for early intervention and improvement of prognosis.

Relationship between changes in neurological deficit severity and adverse cardiac events in elderly patients with hypertensive intracerebral hemorrhage: a retrospective cohort study.

OBJECTIVE: To explore the relationship between changes in neurological deficit severity and the occurrence of adverse cardiac events in elderly patients with hypertensive intracerebral hemorrhage. METHODS: Receiver operating characteristic (ROC) curve analysis was used to evaluate the predictive value of NIHSS scores for adverse cardiac events. RESULTS: There were significant differences between the two groups. Multivariate logistic regression analysis showed that advanced age, high NIHSS score, large intracerebral hemorrhage volume, and high CK level were independent risk factors for adverse cardiac events in elderly patients with hypertensive intracerebral hemorrhage (p < 0.05). The NIHSS scores of both groups gradually increased after admission, peaking at 48 h after admission. In Group A, this elevation persisted until 72 h after admission, while in Group B, there was a significant decrease at 72 h after admission (p < 0.05). From admission to 7 days after admission, the NIHSS scores in Group A were higher than those in Group B (p < 0.05). The area under the curve (AUC) of the NIHSS scores at 48 h after admission was 0.776, with sensitivity and specificity of 80.9% and 84.5%, respectively, which were higher than those of other indicators (p < 0.05). CONCLUSION: The occurrence of adverse cardiac events in elderly patients with hypertensive intracerebral hemorrhage is influenced by multiple factors, and as the NIHSS score increases, the risk of such events gradually increases. Clinicians should pay attention to monitoring NIHSS scores after admission, as they have value in predicting adverse cardiac events in elderly patients with hypertensive intracerebral hemorrhage.

Effects of clinical nursing pathway on surgical site wound infection in patients undergoing acute appendicitis surgery: A meta-analysis.

This study aimed to explore the impact of clinical nursing pathway applied to acute appendicitis surgery on patients' postoperative wound infections and complications. A computerised search of PubMed, Cochrane Library, Web of Science, EMBASE, Wanfang, Chinese Biomedical Literature Database and China National Knowledge Infrastructure was conducted and supplemented by a manual search, from database inception to October 2023, to collect randomised controlled trials (RCTs) on the application of clinical nursing pathways to acute appendicitis surgery. Literature screening, data extraction and quality assessment of the included literature were carried out independently by two researchers. RevMan 5.4 software was applied for data analysis. Twenty-one RCTs with a total of 2408 patients were finally included. The analysis revealed the implementation of clinical nursing pathway could effectively reduce the incidence of wound infection (OR = 0.26, 95% CI: 0.15-0.46, p < 0.001) and postoperative complications (OR = 0.20, 95% CI: 0.15-0.27, p < 0.001), as well as shorten the hospital length of stay (MD = -3.26, 95% CI: -3.74 to -2.79, p < 0.001) and accelerated the time to first ventilations (MD = -14.85, 95% CI: -21.56 to -8.13, p < 0.001), as well as significantly improved patient satisfaction (OR = 5.52, 95% CI: 3.52-8.65, p < 0.001) in patients undergoing surgery for acute appendicitis. The application of clinical nursing pathway in acute appendicitis surgery can significantly reduce postoperative wound infection and complications, and at the same time can shorten the hospital length of stay as well as improve the satisfaction of patients.

Effect of intraoperative abdominal lavage versus suction alone on postoperative wound infection in patients with appendicitis: A meta-analysis.

There is much controversy about the application of abdominal irrigation in the prevention of wound infection (WI) and intra-abdominal abscess (IAA) in the postoperative period. Therefore, we performed a meta-analysis of the effect of suctioning and lavage on appendectomy to assess the efficacy of either suctioning or lavage. Data were collected and estimated with RevMan 5.3 software. Based on our research, we found 563 publications in our database, and we eventually chose seven of them to analyse. The main results were IAA after the operation and WI. Inclusion criteria were clinical trials of an appendectomy with suctioning or lavage. In the end, seven trials were chosen to meet the eligibility criteria, and the majority were retrospective. The results of seven studies showed that there was no statistically significant difference between abdominal lavage and suctioning treatment for post-operative WI (OR, 1.82; 95% CI, 0.40, 2.61; p = 0.96); There was no statistically significant difference between the two groups in the risk of postoperative abdominal abscess after operation (OR, 1.16; 95% CI, 0.71, 1.89; p = 0.56). No evidence has been found that the use of abdominal lavage in the treatment of postoperative infectious complications after appendectomy is superior to aspiration.

[Penehyclidine hydrochloride regulates angiopoietin 2/vascular endothelial cadherin (Ang2/VE-cadherin) pathway to alleviate LPS induced lung injury in rats].

Objective To explore the effect and mechanism of penehyclidine hydrochloride (PHCD) on vascular endothelial injury in septic rats. Methods Fifty male SD rats were randomly divided into control group, lipopolysaccharide (LPS) induced sepsis group (model group), low dose PHCD (0.3 mg/kg) group, medium dose PHCD (1.0 mg/kg) group and high dose PHCD (3.0 mg/kg) groups, ten mice for each group. Normal saline was injected into the tail vein of the control group, and 10 mg/kg lipopolysaccharide (LPS) was injected into the tail vein of the rats in other groups to prepare the sepsis rat models. After the models were successfully established, low, medium and high doses (0.3, 1.0, 3.0 mg/kg) of PHCD solution were injected into the tail vein of the rats of corresponding groups. Wet/dry mass ratio (W/D) of lung tissue of rats in each group was measured, and ELISA was used to assay interleukin-1ß (IL-1ß), tumor necrosis factor-α (TNF-α), IL-6 content and rat plasma angiopoietin 2 (Ang2) content in bronchoalveolar lavage fluid (BALF). HE staining was used to observe the pathological changes of lung tissues. Immunohistochemical staining was used to observe the expression of Ang2 in the right lung tissues. Western blot analysis was performed to detect Ang2 and vascular endothelial cadherin (VE-cadherin) protein in lung tissues. Results Compared with the control group, the W/D ratio of the lung tissues of rats in the model group and the contents of IL-1ß, IL-6 and TNF-α in BALF were significantly increased; the lung tissues showed obvious pathological damage, with up-regulation of Ang2 expression and down-regulation of VE-Cadherin expression. Compared with the model group, the W/D ratio of the lung tissues of rats in three PHCD treatment groups and the contents of IL-1ß, IL-6 and TNF-α in BALF were significantly reduced; the pathological damage of lung tissue was significantly reduced, with down-regulation of Ang2 expression and up-regulation of VE-cadherin expression. Conclusion PHCD can reduce LPS-induced lung inflammation in rats with sepsis by regulating the Ang2/VE-Cadherin pathway, thereby improving vascular endothelial injury.

Silencing ApoC3 alleviates LPS-induced acute lung injury by inhibiting TLR signaling pathway.

This study aims to confirm whether apolipoprotein C3 (ApoC3) can regulate the inflammatory response and tissue damage in acute lung injury (ALI) and explore its regulatory pathway. ALI mouse model was established by intraperitoneal injection of lipopolysaccharide (LPS). ApoC3 levels were detected by real-time quantitative polymerase chain reaction, immunohistochemistry, and western blot assays. The levels of various inflammatory factors were detected by enzyme-linked immunosorbent assay and western blot analysis. Finally, the expression of toll-like receptor (TLR)/nuclear factor kappa B (NF-κB) signaling pathway-related protein [TLR2, myeloid differentiation primary response protein 88 (MyD88), IL-1 receptor-associated kinase 1 (IRAK1), NF-κB p65, and inhibitor of kappa B alpha (IκBα)], SLP adaptor and CSK interacting membrane protein (SCIMP), spleen tyrosine kinase (Syk), and phosphorylated (p)-Syk was detected by western blot analysis. ApoC3 was overexpressed in ALI mouse lung tissue and cell inflammation model. Silencing ApoC3 reduced inflammatory factors and alleviated lung tissue damage in ALI mice. Silencing ApoC3 reduced inflammatory factors and downregulated the expression of TLR2, MyD88, IRAK1, NF-κB p65, and increased IκBα expression in LPS-treated RAW264.7 cells. Moreover, co-transfection of si-TLR2 and shApoC3 further enhanced the inhibitory effects on the levels of inflammatory factors induced by silencing ApoC3. ApoC3 overexpression increased the levels of inflammatory factors and protein expression of SCIMP and p-Syk, while silencing TLR2 reversed the promotive effects of ApoC3 overexpression on above factors. In LPS-induced ALI mouse model and inflammatory cell model, downregulation of ApoC3 reduced inflammatory factors and relieved tissue damage. This process might be achieved through the TLR pathway.

A gene polymorphism at SP-B 1580 site regulates the pulmonary surfactant tension of viral pneumonia through the cellular pyroptosis signaling pathway.

BACKGROUND: Viral pneumonias, such as SARS and MERS, have been a recurrent challenge for the public healthcare system. COVID-19 posed an unprecedented global crisis. The primary impact of viral pneumonia is pathologic changes of lung tissue. However, the effect of SP-B site gene polymorphism on alveolar surface tension in viral pneumonia remains unexplored. OBJECTIVE: To explore the molecular mechanism of how the gene polymorphism at SP-B 1580 site regulates the pulmonary surfactant tension of viral pneumonia through the cellular pyroptosis signaling pathway using an in vivo animal experiment and a clinical trial. METHODS: We constructed a genetically modified mouse model of viral pneumonia and administered H5N1 influenza virus through intratracheal injection. After 48 hours, the survival rate of each mouse group was evaluated. Lung tissue, blood, and bronchoalveolar lavage fluid samples were collected for histopathologic analysis. Inflammatory factor concentrations were measured using ELISA. The level of apoptosis was determined using TUNEL assay. Changes in the expression of cell death-related factors were assessed using qRT-PCR and protein blotting. Additionally, blood samples from patients with viral pneumonia were analyzed to detect single nucleotide polymorphisms and explore their correlation with disease severity, inflammatory factor levels, and pulmonary surfactant protein expression. RESULTS: Following H5N1 infection of mice, the model group and hSP-B-C group showed high mortality rates within 24 hours. The survival rates in the blank control group, virus model group, hSP-B-C group, and hSP-B-T group were 100%, 50%, 37.5%, and 75%, respectively. Histologic analysis revealed significant lung tissue damage, congestion, alveolar destruction, and thickened alveolar septa in the model and hSP-B-C groups. However, these pulmonary lesions were significantly alleviated in the hSP-B-T group. Inflammatory factor levels were elevated in the model and hSP-B-C groups but reduced in the hSP-B-T group. TUNEL assay demonstrated a decrease in apoptotic cells in the lungs of the hSP-B-T group. Furthermore, the expression of SP-B and cell death-related proteins was downregulated in all three groups, with the lowest expression observed in the hSP-B-C group. The clinical trial found that patients with severe viral pneumonia exhibited a higher frequency of CC genotype and C allele in, along with increased inflammatory factor levels and decreased SP-B expression compared to those with mild-to-moderate viral pneumonia. CONCLUSION: SP-B polymorphism at the 1580 site regulates lung surfactant tension through the cell pyroptosis signaling pathway, thus affecting the progression of viral pneumonia.

Regulatory Roles of Human Surfactant Protein B Variants on Genetic Susceptibility to Pseudomonas Aeruginosa Pneumonia-Induced Sepsis.

Surfactant protein B (SP-B) is essential for life and plays critical roles in host defense and lowering alveolar surface tension. A single-nucleotide polymorphism (SNP rs1130866) of human SP-B (hSP-B) alters the N-linked glycosylation, thus presumably affecting SP-B function. This study has investigated the regulatory roles of hSP-B genetic variants on lung injury in pneumonia-induced sepsis. METHODS: Wild-type (WT) FVB/NJ and humanized transgenic SP-B-T and SP-B-C mice (expressing either hSP-B C or T allele without mouse SP-B gene) were infected intratracheally with 50 µL (4 × 10 colony-forming units [CFUs]/mouse) Pseudomonas aeruginosa Xen5 or saline, and then killed 24 or 48 h after infection. Bacterial dynamic growths were monitored from 0 to 48 h postinfection by in vivo imaging. Histopathological, cellular, and molecular changes of lung tissues and bronchoalveolar lavage fluid (BALF) were analyzed. Surface tension of surfactants was determined with constrained drop surfactometry. RESULTS: SP-B-C mice showed higher bioluminescence and CFUs, increased inflammation and mortality, the higher score of lung injury, and reduced numbers of lamellar bodies in type II cells compared with SP-B-T or WT (P < 0.05). Minimum surface tension increased dramatically in infected mice (P < 0.01) with the order of SP-B-C > SP-B-T > WT. Levels of multiple cytokines in the lung of infected SP-B-C were higher than those of SP-B-T and WT (P < 0.01). Furthermore, compared with SP-B-T or WT, SP-B-C exhibited lower SP-B, higher NF-κB and NLRP3 inflammasome activation, and higher activated caspase-3. CONCLUSIONS: hSP-B variants differentially regulate susceptibility through modulating the surface activity of surfactant, cell death, and inflammatory signaling in sepsis.

Interleukin-35 Attenuates D-Galactosamine/Lipopolysaccharide-Induced Liver Injury via Enhancing Interleukin-10 Production in Kupffer Cells.

Interleukin (IL) -35 is an anti-inflammatory cytokine which exerts various beneficial effects on autoimmune diseases. However, whether IL-35 plays a role in endotoxin induced hepatitis demands clarification. This study aims to reveal the effect and mechanism of IL-35 on endotoxin induced liver injury. Acute hepatic injury was induced by D-galactosamine (D-GalN, 400 mg/kg) and lipopolysaccharide (LPS, 5 µg/kg) administration in mice. IL-35 treatment ameliorated D-GalN/LPS induced liver injury in a dose dependent manner as shown by histological examination, ALT determination and Caspase-3 activity assay. It also reduced production of pro-inflammatory cytokines, tumor necrosis factor (TNF)-α, IL-1ß, and IL-6, and increased production of anti-inflammatory cytokines, IL-4, IL-10, and transforming growth factor (TGF)-ß. This hepato-protective effect was proved mainly mediated by Kupffer cells (KC) via gadolinium chloride depletion and cell adoptive transfer experiment. In addition, IL-35 emolliated the cytotoxicity of LPS-triggered KCs to hepatocytes, suppressed nitric oxide (NO) and TNF-α production, and elevated IL-10 production in LPS stimulated KCs. Furthermore, IL-35 could not exert hepato-protective effect in IL-10-deficient mice in vivo and it could not suppress LPS induced NO and TNF-α production in IL-10-deficient KCs in vitro. In conclusion, IL-35 protects endotoxin-induced acute liver injury, which mainly acts thought increasing IL-10 production in KCs. This finding demonstrates a role of IL-35 in anti-infectious immunity and provides a potential therapeutic target in treating fulminant hepatitis.

Identification of protein complexes associated with myocardial infarction using a bioinformatics approach.

Myocardial infarction (MI) is a leading cause of mortality and disability worldwide. Determination of the molecular mechanisms underlying the disease is crucial for identifying possible therapeutic targets and designing effective treatments. On the basis that MI may be caused by dysfunctional protein complexes rather than single genes, the present study aimed to use a bioinformatics approach to identifying complexes that may serve important roles in the development of MI. By investigating the proteins involved in these identified complexes, numerous proteins have been reported that are related to MI, whereas other proteins interacted with MI­related proteins, which implied that these protein complexes may indeed be related to the development of MI. The protein complexes detected in the present study may aid in our understanding of the molecular mechanisms that underlie MI pathogenesis.

Molecular mechanism of miR-181b in heart disease due to pregnancy-induced hypertension syndrome.

The present study aimed to investigate the molecular mechanisms of microRNA (miR)-181b in heart disease due to hypertensive disorders complicating pregnancy (HDCP) through regulating the expression of metallopeptidase inhibitor 3 (TIMP3). miR-181b expression was detected by reverse transcription-quantitative polymerase chain reaction in peripheral blood samples from patients with HDCP. These samples were analyzed for clinical pathological characteristics. The primary cardiomyocytes of rats were cultured in hypoxic conditions for 24 h, in which miR-181b expression was detected at different time points. The expression of TIMP3 was assessed in normal rat cardiomyocytes following transfection with miR-181b mimics by western blot analysis. The TIMP3 protein was also detected in cardiomyocytes following transfection with TIMP3 short interfering-RNA. The apoptosis rate of transfected cardiomyocytes was detected by flow cytometry following 24 h of culture in a hypoxic environment. Luciferase assay was applied to validate whether miR-181b binds to the 3' untranslated region of TIMP3 mRNA. miR-181b expression was significantly downregulated in the peripheral blood of patients with HDCP and the miR-181b expression was negatively associated with the grades of hypertension (P<0.05). The results of luciferase assay indicated that miR-181b directly targets TIMP3. The apoptosis rates of rat cardiomyocytes in the group transfected with miR-181b or TIMP3 siRNA was significantly lower than the normal control group (P<0.05). miR-181b may inhibit apoptosis of cardiomyocytes to protect myocardial cells through directly targeting TIMP3 genes, which serve important roles in HDCP.

Homocysteine injures vascular endothelial cells by inhibiting mitochondrial activity.

The aim of the present study was to investigate the role of homocysteine (Hcy) in the pathogenesis of pulmonary embolism (PE) and the associated molecular mechanisms in human umbilical vein endothelial cells (HUVECs). Hcy contents were detected with high-performance liquid chromatography. Apoptosis was detected by flow cytometry using Annexin-V staining. Cytochrome c oxidase (COX) activity was assessed with an enzyme activity assay, and the expression levels of COX 17 were determined by western blot analysis. Intracellular reactive oxygen species levels were measured using a microplate reader with a fluorescence probe. The results demonstrated that, compared with the control group, the serum Hcy levels were significantly elevated in the PE group, suggesting that Hcy may be an indicator for PE. Following treatment with Hcy, the apoptosis rate was markedly elevated in HUVECs. Moreover, Hcy decreased COX activity and downregulated the expression of COX 17 in HUVECs. Furthermore, Hcy increased the ROS levels in these endothelial cells. However, all the above-mentioned physiopathological changes induced by Hcy in HUVECs could be restored by folic acid. In conclusion, the results of the present study demonstrated that Hcy inhibited COX activity, downregulated COX 17 expression, increased intracellular ROS levels and enhanced apoptosis in endothelial cells.

Serum protein biomarkers screening in patients with ischemic stroke by LC-MS/MS.

BACKGROUND: The purpose of this study was to investigate the serum proteins biomarkers by label-free liquid chromatography coupled to tandem mass spectrometry quantification methods in the Chinese patients with acute ischemic stroke (AIS). METHOD: In the study period, sera from 40 AIS patients and 40 normal cases were selected for screening study. The selected protein associations with disease risk were further evaluated by enzyme-linked immunosorbent assay (ELISA) testing of the remaining stroke cases and controls. Its value for biomarkers diagnosis was appreciated through receiver operating characteristic (ROC) curve. RESULTS: Patients versus control levels differences were suggested for 19 proteins (nominal P < 0.05) for stroke, with three proteins having a false discovery rate <0.05. The association of mannose-binding lectin (MBL) with stroke (P < 0.001) was confirmed using ELISA in replication studies. Based on the ROC curve, the optimal serum concentration of MBL as a surrogate marker to support the diagnosis of ischemic cerebral injury was found to be 1050 ug/L, which yielded a sensitivity of 81.8% and a specificity of 80.2%, the area under the curve was 0.812 (95% CI: 0.724-0.876). In multivariate analysis, there was an increased risk of AIS associated with MBL levels ≥1050 ug/L (OR: 4.76, 95% CI: 1.59-10.12) after adjusting for possible confounders. CONCLUSION: The discovery and replication studies presented here show MBL to be a risk marker for AIS in the Chinese population, which appears to be a novel finding.

Identify asthma genes across three phases based on protein-protein interaction network.

Asthma is a common inflammatory disease that is generally caused by genetic mutations or environmental factors. Recently, the emerging of omics data provides an alternative way to understand asthma. In this study, the authors present a new framework to detect asthma disease genes based on protein-protein interaction network (PPIN) and gene expression. Specifically, they construct PPINs for different stages of asthma, and detect those interactions occurred in the specific stages. By investigating the proteins in these stage-specific interactions, they find they are more likely related to asthma, and the functional enrichment analysis indicate that the pathways enriched in the differential interactions are related to the progress of asthma. Moreover, some proteins in the differential interactions have been previously reported to be related to asthma in the literature, implying the usefulness of the proposed approach.

Hydrogen sulfide endothelin-induced myocardial hypertrophy in rats and the mechanism involved.

The aim of the study was to evaluate the clinical efficacy of hydrogen sulfide (H2S) treatment on the endothelin-induced cardiac hypertrophy. Sixty-four adult male rats, weighing from 180 to 200 g, were randomly divided into four groups: ten in normal group, ten in sham group, 44 in model group established by inducing the myocardial hypertrophy with endothelin. The myocardial hypertrophy model rats were randomly divided into two groups: 22 in the simple myocardial hypertrophy model group and 22 in the H2S treatment group. Rats in normal group were given 2 ml pure water by gavage per day, those in the sham group and simple cardiac hypertrophy model group were given 2 ml of saline by gavage per day, and rats in the pure cardiac hypertrophy with H2S treatment were given intraperitoneal injections of 2 ml NaHS saline per day for a period of 4 weeks. Left ventricular mass index, myocyte hypertrophy, volume fraction of myocardial interstitial collagen, myocardial hydroxyproline content and other indicators of cardiac hypertrophy were observed after 4 weeks. (1) There were significant differences on the ventricular mass between the treatment group and the cardiac hypertrophy group: The left ventricular mass decreased 21.4 % and the left ventricular mass index decreased 5.97 % (P < 0.05; (2) the smallest cardiomyocytes diameter and cardiomyocytes cross-sectional area decreased 12.5 and 10.8 %, respectively (P < 0.05) in the treatment group compared to the cardiac hypertrophy group; (3) the volume fraction of myocardial interstitial collagen and the myocardial hydroxyproline content decreased 22.3 and 31.3 % in treatment group compared with the cardiac hypertrophy group, respectively (P < 0.05). H2S had a good clinical efficacy in reducing left ventricular mass fraction and myocardial collagen levels, improving myocardial hypertrophy and decrease myocardial fibrosis. It is worthy for further clinical studies.