Application of Indian ink markers for locating gastric varices under endoscopic ultrasonography.

OBJECTIVE: The present study aimed to investigate the accuracy of endoscopic ultrasonography (EUS) combined with Indian ink in locating target vessels of gastric varices (GVs) compared with conventional endoscopic techniques. Additionally, the characteristics of GVs under conventional endoscopy were also explored. METHODS: All 50 cirrhotic patients with GVs between August 2021 and December 2022 were included in the study. Firstly, conventional endoscopy was employed to identify GVs and to record the expected injection sites. Subsequently, EUS was used to locate the perforated vessel and the injection site was them marked with India ink followed by injection with cyanoacrylate (CYA). Finally, conventional endoscopy was used to examine GVs, to identify the marker points of Indian ink and to compare whether the injection points under conventional endoscopy were consistent with those marked with Indian ink. Furthermore, patients with consistent and inconsistent distribution of endoscopic markers and injection sites were divided into two groups. RESULTS: EUS could detect the perforating vessels in real time and intuitively. The distribution of markers using EUS was significantly different compared with the injection points obtained by conventional endoscopy (P < 0.001). Therefore, 20 cases were allocated to the consistent group and 30 cases to the non-consistent group. 16 patients who showed red wale signs were obtained in the consistent group and 11 patients in the non-consistent group (P = 0.048). The diameter of the largest GVs was 13.5 (10-15) mm in the consistent group compared with 10 (7.5-10) mm in the non-consistent group (P = 0.006). CONCLUSION: EUS could provide the exact location of GVs, thus more accurately describing the endoscopic characteristics of the GVs. Furthermore, the red wale signs and diameter of the largest GVs obtained using conventional endoscopy were helpful in determining the location of target GVs.

High-precision nanosecond detection of a gas absorption spectrum based on optical frequency comb time-frequency mapping.

There is an increasing demand for high-precision gas absorption spectroscopy in basic research and industrial applications, such as gas tracking and leak warning. In this Letter, a novel, to the best of our knowledge, high-precision and real-time gas detection method is proposed. A femtosecond optical frequency comb is used as the light source, and a broadening pulse containing a range of oscillation frequencies is formed after passing through a dispersive element and a Mach-Zehnder interferometer. Four absorption lines of H13C14N gas cells are measured at five different concentrations within a single pulse period. A single scan detection time of only 5 ns is obtained along with a coherence averaging accuracy of 0.0055 nm. High-precision and ultrafast detection of the gas absorption spectrum is accomplished while overcoming complexities related to the acquisition system and light source that are encountered in existing methods.

Efficient Initial Eradication of Large Esophageal Varices by Balloon-compression Endoscopic Injection Sclerotherapy.

BACKGROUND: The management of large esophageal varices (EVs) remains challenging because of the difficulty of endoscopic variceal ligation and fatal post-endoscopic variceal ligation bleeding ulcers. The current study evaluated the efficacy and safety of balloon-compression endoscopic injection sclerotherapy (bc-EIS) in the treatment of large EVs. MATERIALS AND METHODS: This retrospective study included 105 patients with cirrhosis exhibiting large EVs (64 in the bc-EIS group and 41 in the EIS group). Primary outcomes included the initial rate of variceal eradication and intraoperative bleeding signs. Secondary outcomes included incidences of rebleeding, mortality, complications, and optimal time of balloon-compression (bc). RESULTS: The initial rate of variceal eradication in the bc-EIS group was significantly higher than that in the EIS group (46.9 vs. 24.4%; P =0.021). The incidence of intraoperative bleeding, which was represented as oozing and spurting, in the bc-EIS group was markedly lower than that in the EIS group (43.8 vs. 61.0% and 9.4 vs. 39.0%, respectively; P =0.043). Patients in the bc-EIS group showed a significantly lower incidence of rebleeding (0.0 vs. 17.1%; P =0.001). However, no significant difference in mortality rate was observed between different groups. Chest pain or discomfort tended to be more common in the EIS group than in the bc-EIS group (58.5 vs. 17.2%; P =0.001). The cut-off value of 11.5-minutes appeared to have a maximum combined sensitivity and specificity of 80.0% and 58.8%, respectively. The area under the curve was 0.708 (95% confidence interval =0.576-0.839; P =0.004). CONCLUSION: bc-EIS could achieve a higher variceal eradication rate and milder intraoperative bleeding signs in large EVs. Furthermore, 11.5-minutes appeared to be the optimal compression time in bc-EIS.

Novel balloon compression-assisted endoscopic injection sclerotherapy and endoscopic variceal ligation in the treatment of esophageal varices: a prospective randomized study.

BACKGROUND: Herein, our group designed a novel technology, termed balloon compression-assisted endoscopic injection sclerotherapy (bc-EIS), which was applied to improve the efficiency of eradicating esophageal varices (EVs). The present study aimed to compare the rate of eradication and efficacy between bc-EIS and endoscopic variceal ligation (EVL) in the management of EVs. METHODS: Ninety-five patients with esophageal variceal bleeding (EVB) were randomly assigned to receive bc-EIS or ligation alone. Additional treatment sessions were held 1 month later and then at 3-month intervals until eradication of the varices was achieved. Endoscopic follow-up examinations were carried out at 6-month intervals in the absence of recurrence or immediately if there was any recurrent bleeding. RESULTS: The mean physical injection points per session were 2.89 ± 0.79, and the mean volume of lauromacrogol used per session was 17.74 ± 7.09 ml in the bc-EIS group. The mean band per session was 6.13 ± 0.86. The rate of eradication after one to three rounds of bc-EIS was obviously higher than that of the EVL group (89.36%, 97.87%, and 100% vs. 37.5%, 43.75%, and 47.92%, respectively). Retrosternal pain or discomfort in the bc-EIS group was slightly lower than that in the EVL group (23.4%, 11/47 vs. 31.25%, 15/48). Two and five patients showed mild abdominal bloating and distension between the bc-EIS and EVL groups, respectively (2/47, 4.26% vs. 5/48, 10.42% P > 0.05). Nausea and vomiting were reported in one patient (1/47, 2.13%) in the bc-EIS group and three patients (3/48, 6.25%) in the EVL group. However, there were no statistically significant differences between the two groups (P > 0.05). No fatal or severe complications, such as esophageal perforation, esophageal stricture or ectopic embolism, were observed. CONCLUSION: The bc-EIS method was effective in eradicating EVs and was accompanied by fewer complications.

Integrative analysis of miRNA and mRNA expression profiles reveals a novel mRNA/miRNA signature to improve risk classification for patients with gastric cancer.

Gastric cancer (GC) is one of the most common types of malignant cancer and is associated with poor prognosis. Although the prognosis of patients with GC is associated with grade, stage and lymph node metastases, these traditional clinical features are inadequate to predict the outcome of GC. Therefore, there has been an increased focus on identifying novel molecular biomarkers for early diagnosis and prognosis, in order to improve outcomes in GC. In the present study, an integrative analysis of microRNA (miRNA) expression profiles, mRNA expression profiles and clinical characteristics was performed in a large cohort of patients with GC in order to identify an integrative prognostic model for improving postoperative risk classification. An integrative mRNA/miRNA signature (IMMIS), comprised of three miRNAs and one mRNA, was identified from a large number of differentially expressed miRNAs and mRNAs using univariate and multivariate Cox regression analysis. The prognostic value of the IMMIS was validated in the discovery cohort, testing cohort and The Cancer Genome Atlas (TCGA) cohort. The present results suggested that the identified signature had a reliable predictive performance and could classify the patients into high- and low-risk groups with significantly different overall survival times. In the discovery cohort, the hazard ratio (HR) was 2.805 with a 95% CI=1.722-4.567 (P<0.001). The median overall survival time as 1.49 vs. 3.85 years. In the testing cohort, the HR was 1.625 with a 95% CI=1.004-2.638 (P=0.039) and the median overall survival time was 2.17 vs. 4.62 years. In the TCGA cohort, the HR was 2.139 with a 95% CI=1.519-3.012 (P<0.001) and the median overall survival time was 1.53 vs. 4.62 years. The IMMIS constituted a reliable independent prognostic factor compared with clinical covariates, including age, sex, grade and stage, as indicated by multivariate and stratified analyses. Furthermore, comparative analysis revealed that the predictive value of the IMMIS was superior to the mRNA-based signature alone. The present results suggested the potential value of the IMMIS as a promising novel biomarker for improving the clinical management of patients with GC.

Transcriptome analysis reveals dysregulated long non-coding RNAs and mRNAs associated with extrahepatic cholangiocarcinoma progression.

The incidence of extrahepatic cholangiocarcinoma (ECC) is the highest of all the cholangiocarcinoma cases. However, the molecular mechanism of ECC genesis and progression remains unclear. Long non-coding RNAs (lncRNAs) have been revealed to perform critical regulatory roles in cancer biology. In order to understand lncRNA expression patterns and their potential function in ECC, a transcriptome analysis of lncRNA and mRNA expression was performed in ECC and paired adjacent non-cancerous tissues using Agilent human lncRNA + mRNA arrayV4.0 (4×180 K format). It was identified that 268 lncRNAs and 459 mRNAs were differentially expressed in ECC. Among these, 78 lncRNAs and 66 mRNAs were upregulated >2-fold compared with adjacent non-cancerous tissues, and 190 lncRNAs and 393 mRNAs were downregulated in the ECC samples. Differences in lncRNA expression between ECC and paired adjacent non-cancerous tissues were confirmed using reverse transcription-quantitative polymerase chain reactionas proof of principle. Functional analysis of co-expressed mRNAs with lncRNAs indicated that these dysregulated lncRNAsmay be involved in known ECC-associated biological processes and pathways. The present findings indicated that mRNAs and lncRNAs perform important roles in the development and progression of ECC. The present findings may lay the foundation for future efforts to understand the role of lncRNAs and develop novel biomarkers in ECC.

The prognostic potential and carcinogenesis of long non-coding RNA TUG1 in human cholangiocarcinoma.

Cholangiocarcinoma (CCA) is a fatal disease with increasing worldwide incidence and is characterized by poor prognosis due to its poor response to conventional chemotherapy or radiotherapy. Long non-coding RNAs (lncRNAs) play key roles in multiple human cancers, including CCA. Cancer progression related lncRNA taurine-up-regulated gene 1 (TUG1) was reported to be involved in human carcinomas. However, the impact of TUG1 in CCA is unclear. The aim of this study was to explore the expression pattern of TUG1 and evaluate its clinical significance as well as prognostic potential in CCA. In addition, the functional roles of TUG1 including cell proliferation, apoptosis, migration, invasion and epithelial-mesenchymal transition (EMT), were evaluated after TUG1 silencing. Our data demonstrated up-regulation of TUG1 in both CCA tissues and cell lines. Moreover, overexpression of TUG1 is linked to tumor size (p=0.005), TNM stage (p=0.013), postoperative recurrence (p=0.036) and overall survival (p=0.010) of CCA patients. Furthermore, down-regulation of TUG1 following RNA silencing reduced cell growth and increased apoptosis in CCA cells. Additionally, TUG1 suppression inhibited metastasis potential in vitro by reversing EMT. Overall, our results suggest that TUG1 may be a rational CCA-related prognostic factor and therapeutic target.

Long noncoding RNA PCAT1 regulates extrahepatic cholangiocarcinoma progression via the Wnt/ß-catenin-signaling pathway.

Extrahepatic cholangiocarcinoma (ECC) is a deadly disease that often responds poorly to conventional chemotherapy or radiotherapy. Long noncoding RNAs (lncRNAs) play important roles in human cancers, including ECC, and recent studies indicated that the lncRNA prostate cancer-associated transcript 1 (non-protein coding) (PCAT1) is involved in multiple cancers. However, the role of PCAT1 in ECC is unclear. Previously, we showed that PCAT1 is up-regulated in both ECC tissue samples and cell lines. Here, we showed that downregulation of PCAT1 following transfection with silencing RNA reduced ECC cell growth and increased cell apoptosis. Additionally, PCAT1 suppression inhibited ECC cell migration and invasion as determined by transwell assay. Furthermore, we determined that PCAT1 is a competing endogenous for microRNA (miR)-122, with bioinformatics analysis and luciferase-reporter assay results demonstrating that PCAT1 regulated WNT1 expression via miR-122. Moreover, PCAT1 downregulation increased levels of glycogen synthase kinase 3ß and significantly decreased ß-catenin levels in whole cell lysates and nuclear fractions, indicating that PCAT1 silencing inhibited the Wnt/ß-catenin-signaling pathway. We also observed that exogenous expression of WNT1 reversed PCAT1-silencing-induced inhibition of ECC cell growth inhibition. These results indicated that PCAT1 silencing inhibited ECC progression by reducing Wnt/ß-catenin signaling through miR-122 repression and WNT1 expression. Our findings revealed an important role of PCAT1 in ECC and suggested that PCAT1 might be a potential ECC-related therapeutic target.

Iron(iii) chloride hexahydrate-promoted selective hydroxylation and chlorination of benzyl ketone derivatives for the construction of hetero-quaternary scaffolds.

A novel and tunable α-hydroxylation/α-chlorination of benzyl ketone derivatives has been developed for the construction of hetero-quaternary carbon centers by iron(iii) chloride hexahydrate mediated selective transformations through the application of different oxidants, especially the crystal water in the catalyst as an OH source is firstly reported in this hydroxylation.

Iron-Catalyzed α-Arylation of Deoxybenzoins with Arenes through an Oxidative Dehydrogenative Approach.

A novel α-arylation of deoxybenzoins with non-prefunctionalized arenes is developed through an iron-catalyzed oxidative dehydrogenative approach. The reaction shows broad substrate scope and functional group tolerance and thus provides efficient access to synthetically useful 1,2,2-triarylethanones. A reasonable mechanism is also proposed.

Identifying survival-associated ceRNA clusters in cholangiocarcinoma.

Competing endogenous RNAs (ceRNAs) represent a novel layer regulations of long non-coding RNAs (lncRNAs) and genes that play important roles in cancer pathogenesis by binding microRNAs (miRNAs). However, the competition mechanism of ceRNAs in cholangiocarcinoma (CHOL) is not fully understood. In this study, we constructed a dysregulated ceRNA competitive network (CCEN) to globally characterize the competing difference between CHOL and normal tissues. Then, we integrated affinity propagation and Kaplan­Meier (K-M) methods to identify functional clusters associated with survival. A total of 7 key ceRNA clusters were identified. Further functional annotation analyses found that Cluster23 and Cluster32 involved cell based functions, and the loss of ceRNA competitive relations in clusters may contribute to CHOL, by disturbing important biological processes, such as 'Pathway in cancer', MAPK and Neurotrophin signaling pathway. This study provides further insights into understanding the competitive mechanism of ceRNAs in CHOL.

Divergence in Enzymatic Activities in the Soybean GST Supergene Family Provides New Insight into the Evolutionary Dynamics of Whole-Genome Duplicates.

Whole-genome duplication (WGD), or polyploidy, is a major force in plant genome evolution. A duplicate of all genes is present in the genome immediately following a WGD event. However, the evolutionary mechanisms responsible for the loss of, or retention and subsequent functional divergence of polyploidy-derived duplicates remain largely unknown. In this study we reconstructed the evolutionary history of the glutathione S-transferase (GST) gene family from the soybean genome, and identified 72 GST duplicated gene pairs formed by a recent Glycine-specific WGD event occurring approximately 13 Ma. We found that 72% of duplicated GST gene pairs experienced gene losses or pseudogenization, whereas 28% of GST gene pairs have been retained in the soybean genome. The GST pseudogenes were under relaxed selective constraints, whereas functional GSTs were subject to strong purifying selection. Plant GST genes play important roles in stress tolerance and detoxification metabolism. By examining the gene expression responses to abiotic stresses and enzymatic properties of the ancestral and current proteins, we found that polyploidy-derived GST duplicates show the divergence in enzymatic activities. Through site-directed mutagenesis of ancestral proteins, this study revealed that nonsynonymous substitutions of key amino acid sites play an important role in the divergence of enzymatic functions of polyploidy-derived GST duplicates. These findings provide new insights into the evolutionary and functional dynamics of polyploidy-derived duplicate genes.

Metformin inhibits tumor growth by regulating multiple miRNAs in human cholangiocarcinoma.

The antidiabetic drug metformin exerts antineoplastic effects in many types of malignancies, however the effect of metformin on cholangiocarcinoma (CCA) still remains unclear. In the present study, we investigated that metformin treatment was closely associated with the clinicopathologic characteristics and improved postoperative survival of CCA patients. Metformin inhibited CCA tumor growth by cell cycle arrest in vitro and in vivo. We explored that the expression of six miRNAs (mir124, 182, 27b, let7b, 221 and 181a), which could directly target cell-cycle-regulatory genes, was altered by metformin in vitro and in vivo. These miRNAs were dysregulated in cholangiocarcinoma and promoted the CCA genesis and metformin exactly modulated these carcinogenic miRNAs expression to arrest the cell cycle and inhibit the proliferation. Meanwhile, these miRNAs expression changes correlated with the tumor volume and postoperative survival of CCA patients and could be used to predict the prognosis. Further we confirmed that metformin upregulated Drosha to modulate these miRNAs expression. Our results elucidated that metformin inhibited CCA tumor growth via the regulation of Drosha-mediated multiple carcinogenic miRNAs expression and comprehensive evaluation of these miRNAs expression could be more efficient to predict the prognosis. Moreover, metformin might be a quite promising strategy for CCA prevention and treatment.

A nickel-mediated oxidative α-C(sp(3))-H functionalization of amides with allylic alcohols terminated by radical 1,2-aryl migration.

A Ni-mediated oxidative C(sp(3))-H functionalization of N,N-substituted amides with α,α-diaryl allylic alcohols through a radical 1,2-aryl migration process has been developed. This process features a broad substrate scope and excellent functional group tolerance. Notably, γ-amino ketones containing an all-carbon quaternary center were synthesized under these conditions in moderate to good yields.

Nine-year follow-up of local implantation of autologous skeletal myoblasts in a patient with coronary heart disease.

PATIENT: gender - Male, age - 63 year-old. PRIMARY DIAGNOSIS: Acute myocardial infarction. CO-EXISTING DISEASES: Hypertension. MEDICATION: Aspirin • beta-blocker • captopril. CLINICAL PROCEDURE: CABG • autologous skeletal myoblast transplantation • PCI. SPECIALTY: Cardiology. OBJECTIVE: Unusual or unexpected effect of treatment. BACKGROUND: Cell transplantation has been viewed as a promising strategy for end-stage heart failure, but long-term follow-up results are lacking. CASE REPORT: In December 2002 we began transplanting autologous skeletal myoblasts in one patient because of serious coronary heart disease. Here, we present the 9-year follow-up results of this patient. No ventricular tachyarrhythmias were detected after treatment. The patient had another myocardial infarction in April 2012 and was treated successful with PCI. CONCLUSIONS: Autologous skeletal myoblast transplantation with bypass surgery is associated with improvement in cardiac function and lack of adverse effects in long-term follow-up, making it a promising therapy for patients with heart failure.

Simvastatin augments the efficacy of therapeutic angiogenesis induced by bone marrow-derived mesenchymal stem cells in a murine model of hindlimb ischemia.

Many studies showed beneficial effects of either statin or bone marrow-derived mesenchymal stem cells (MSC) treatment in ischemic disease. In an attempt to further improve postischemic tissue repair, we investigated the effect of a local administration of MSC, in the presence or not of low-dose simvastatin, on angiogenesis and functional recovery in a mouse model of hindlimb ischemia. In vitro, the proliferation, migration, apoptosis, and tube formation of bone marrow MSC derived from transgenic mice expressing green fluorescent protein (GFP) were detected in the presence or not of 0.01 µmol/l simvastatin, respectively. In vivo, immediately after hindlimb ischemia, the mice were divided into four groups, namely control, MSC, statin, and statin-MSC, and received a single local injection of MSC (2×10(6) cells) and/or a repeated gavages' administration of simvastatin (0.2 mg/kg) for 21 days. The blood flow was measured by laser Doppler imaging, the capillary density was detected by alkaline phosphatase staining and, the MSC differentiation was assessed by immunofluorescent staining at 21 days after the ischemia. In vitro, the MSC proliferation rate, migration ability and tube formation number were increased significantly in simvastatin group relative to control group. Whereas, the H2O2 induced-apoptosis was inhibited significantly in simvastatin group relative to control group. In vivo, hindlimb blood reperfusion was significantly improved (MSC 0.55±0.08, statin 0.57±0.05, vs. control 0.47±0.07, P<0.05) and capillary density was obviously higher at day 21 post-ischemia by Laser Doppler Imaging in the MSC group and the Statin group when compared with control group. The combined use of statin and MSC further improved revascularization (perfusion ratio of 0.70±0.09; P<0.001 verse other groups) and resulted in the highest capillary density (P<0.05 vs. all other groups). GFP-labeled transplanted cells were more frequently observed in the Statin-MSC group than in the MSC group (6.8±0.5-3.1±0.7, P<0.05). Low-dose simvastatin could act in a synergistic way with MSC to potentiate the functional neovascularization in a mouse model of hind limb ischemia.

Direct Sp3α-C-H activation and functionalization of alcohol and ether.

Seven kinds of sp(3)α-C-H activation/C-C formation reactions of alcohols and ethers have been reviewed in this tutorial review, from the viewpoint of both methodology and synthetic application, towards the efficiency, chemo-, regio- and stereoselectivity, catalytic system, substrate scope and mechanistic study. Section 2 describes radical-mediated α-C-H activation and addition/elimination of ethers with unsaturated (C=C and C[triple bond]C) species. Sections 3-8 discuss the α-C-H activation and additions of alcohols and/or ethers with unsaturated (C=C, C[triple bond]C, C=O and C=N) compounds, which involve the key processes of radical mediation, carbenoid insertion, 1,5-H-migration, oxidative dehydrogenation coupling, transfer hydrogenative coupling, and metal-mediated C=C insertion into the C-H bond.

Zinc supplementation results in improved therapeutic potential of bone marrow-derived mesenchymal stromal cells in a mouse ischemic limb model.

BACKGROUND AIMS: We wanted to determine whether zinc supplementation can inhibit bone marrow-derived mesenchymal stromal cell (MSC) apoptosis and enhance their tissue regenerative potential a in mouse ischemic hindlimb model. METHODS: Rat bone marrow cells were cultured and the resulting MSC were passaged for 3-7 generations. The proliferation and apoptosis of MSC was examined by 3-[4,5-dimethyl-2-thiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis. The activation of protein kinases B (Akt) was determined by Western blots. Vascular endothelial growth factor (VEGF) levels were examined by enzyme-linked immunosorbent assay. The mouse hindlimb ischemic model was established by ligating the right femoral artery. Mice received MSC, zinc-treated MSC or vehicle. The blood flow was assessed by laser Doppler imaging. The survival rate of donor cells was quantified by real-time polymerase chain reaction for the sex-determining region of the Y-chromosome (Sry). Angiogenesis was assessed by histochemical staining and immunofluoresence staining. RESULTS: Supplementation with physiologic amounts of zinc caused a marked attenuation of cell apoptosis, enhanced cell viabilities, increased VEGF release and up-regulated Akt activation. Zinc-treated MSC delivered into ischemic hindlimbs resulted in significant improvements in limb blood perfusion by increased implanted MSC survival and stimulated angiogenesis. CONCLUSIONS: This study demonstrates the potential of zinc supplement to enhance survival of engrafted MSC and ameliorate their tissue regenerative potential in a mouse ischemic hindlimb model.

Lipopolysaccharide pretreatment protects against ischemia/reperfusion injury via increase of HSP70 and inhibition of NF-κB.

It has been reported that pretreatment of rats with lipopolysaccharide (LPS) increases myocardial functional recovery in ischemia/reperfusion (I/R) hearts. However, the mechanisms by which LPS induces cardioprotection against I/R injury have not been fully elucidated. In this study, we pretreated rats with LPS (1.0 mg/kg) 24 h before they were subjected to I/R injury, and then examined the roles of heat shock protein-70 (HSP70) and nucleus factor-κB (NF-κB) in LPS-induced cardioprotection. We observed that pretreatment with low-dose LPS resulted in significantly increased levels of HSP70 in the myocardium, which could dramatically inhibit NF-κB translocation and reduce degradation of inhibitory κB. Inhibition of NF-κB, in turn, attenuated release of inflammatory cytokines (tumor necrosis factor-α, interleukin (IL)-1ß, and IL-6) and reduced apoptosis of myocardium and infarct area following I/R injury. Moreover, HSP70 could ameliorate oxidative stress following I/R injury. To further investigate whether increase of HSP70 might be responsible for protection of the myocardium against I/R injury, we co-administered the HSP70 inhibitor, quercetin, with LPS before I/R injury. We found that LPS-induced cardioprotection was attenuated by co-administration with quercetin. Herein, we concluded that increased levels of HSP70 through LPS pretreatment led to inhibition of NF-κB activity in the myocardium after I/R injury. Our results indicated that LPS-induced cardioprotection was mediated partly through inhibition of NF-κB via increase of HSP70, and LPS pretreatment could provide a means of reducing myocardial I/R injury.