Correlations of IL-1 and IL-6 Gene polymorphisms with hypertrophic cardiomyopathy.

The purpose of this study was to explore the correlations of interleukin-1 (IL-1) and IL-6 gene polymorphisms with hypertrophic cardiomyopathy (HCM). A total of 200 patients with HCM were enrolled as disease group, and 200 healthy individuals were included as control group. Peripheral blood was collected from all subjects in both disease and control groups. Gene polymorphisms and serum expression levels of IL-1 and IL-6 were detected, and conjoint analysis was performed based on results of cardiac color Doppler ultrasound examination. The allele distribution of IL-1 rs1878320 showed a difference between disease and control groups (P=0.000). The frequency of the allele T was lower in disease group. The genotype distribution of IL-1 rs1878320 (P=0.001) and IL-6 rs1474347 (P=0.000) in disease group was different from that in control. The frequency of TC genotype of IL-1 rs1878320 was lower in disease group, and that of CA genotype of IL-6 rs1474347 was higher in disease group. There was a difference in the distribution of the dominant model of IL-6 rs1474347 between disease and control groups (P=0.021), and the frequency of CC + CA in the dominant model was 171 (0.855). The frequency of AC haplotype of IL-1 gene was overtly higher in disease group (P=0.000), while the frequency of AT haplotype was lower in disease group (P=0.000). The IL-1 rs1516792 polymorphism had an association with serum IL-1 level (P<0.05), the IL-1 level was notably increased in the patients with the genotype AA, and it was higher in disease group. The polymorphism of rs1878320 locus in IL-1 gene was correlated with interventricular septal (IVS) (P=0.047), and IVS was reduced in the patients with TC genotype. The polymorphism of rs1516792 locus in IL-1 gene was distinctly related to left ventricular outflow tract (LVOT) (P=0.041), and LVOT was lowered in the patients with GG genotype. The IL-6 rs2069831 polymorphism was associated with left ventricular ejection fraction (LVEF) (P=0.035), and LVEF declined in the patients with TT genotype. The IL-1 and IL-6 gene polymorphisms are correlated with the susceptibility and progression of HCM.

Effects of steroidal saponins extract from Ophiopogon japonicus root ameliorates doxorubicin-induced chronic heart failure by inhibiting oxidative stress and inflammatory response.

CONTEXT: Ophiopogonis Radix, the root of Ophiopogon japonicus (Thunb.) Ker-Gawl (Liliaceae), is a Traditional Chinese Medicine, which has been investigated to possess effective treatment of cardiovascular diseases. OBJECTIVE: This study evaluates the cardioprotective effects of steroidal saponins extract from Ophiopogon japonicus (SOJ) root against doxorubicin-induced chronic heart failure (CHF) through the amelioration of oxidative stress and inflammation. MATERIALS AND METHODS: A Sprague-Dawley rat model of CHF was established by intraperitoneally injected with DOX. All rats were randomly divided into four groups: Control group, CHF group, CHF + SOJ (100 mg/kg) treatment group, SOJ (100 mg/kg) treatment group (n = 8/group). After six weeks administration, biometric and echocardiography were measured. The levels of biochemical parameters were measured using commercial kits. RESULTS: The values of LVESP, +dP/dtmax, -dP/dtmax, EF and FS increased to 116.20 ± 1.68 mmHg, 2978.71 ± 168.26 mmHg/s, 3452.61 ± 286.09 mmHg/s, 68.26 ± 5.28% and 31.97 ± 3.79%, respectively; the values of LVEDP, LVESD and LVEDD decreased to 8.85 ± 0.84 mmHg, 8.39 ± 0.45 mm and 12.36 ± 0.87 mm in CHF + SOJ group. In addition, the levels of IL-6, TNF-α and IL-1ß decreased to 154.41 ± 7.72 pg/mg protein, 110.02 ± 6.96 pg/mg protein and 39.39 ± 5.27 pg/mg protein, respectively; the relative activity of p38 MAPK decreased to 2.60 ± 0.40 in CHF + SOJ group. Furthermore, the activities of SOD, CAT and GSH-Px increased to 268.77 ± 6.20 U/mg protein, 13.68 ± 0.68 U/mg protein and 316.90 ± 8.08 µmol/mg protein, and the content of MDA decreased to 4.03 ± 0.43 nmol/mg protein in CHF + SOJ group. CONCLUSIONS: SOJ exerts the cardioprotective effect against DOX-induced CHF through suppressing inflammatory and oxidative stress. These results provide evidence that SOJ might be an effective treatment for CHF.

[Retracted] LncRNA TUG1 serves an important role in hypoxia­induced myocardial cell injury by regulating the miR­145­5p­Binp3 axis.

Following the publication of this article, a concerned reader drew to the Editor's attention that, for several of the figures showing the results of Transwell migration and invasion assay experiments, unexpected areas of similarity were identified in terms of cellular patterns comparing among data panels where the results from differently performed experiments were intended to have been shown, although the areas immediately surrounding these areas often featured comparatively different distributions of cells. Moreover, several of the figures contained invasion/migration assay data that were strikingly similar to data that had appeared in articles published previously by different authors at different research institutes. In addition, the western blots in this article were presented with atypical, unusually shaped and possibly anomalous protein bands in many cases. After having conducted an internal investigation, the Editor of Molecular Medicine Reports has reached the conclusion that the potentially anomalous data in this paper were unlikely to have arisen by coincidence. Therefore, on the grounds of a lack of confidence in the integrity of these data, and given the fact that some of the data were strikingly similar to that which had been published previously in other articles and journals, the Editor has decided that the article should be retracted from the publication. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused, and thanks the concerned reader for drawing this matter to our attention. [Molecular Medicine Reports 42: 2422­2430, 2018; DOI: 10.3892/mmr.2017.8116].

LncRNA TUG1 serves an important role in hypoxia-induced myocardial cell injury by regulating the miR­145­5p­Binp3 axis.

The aim of the present study was to investigate the function of long non­coding RNA TUG1 in hypoxia­induced myocardial cell injury and to explore the potential molecular mechanisms. The cardiomyocyte cell line H9c2 was cultured under hypoxic and normoxic conditions. TUG1 expression under hypoxic conditions was then detected. The effects of TUG1 overexpression on viability, apoptosis, migration and invasion were assayed. In addition, the microRNA (miR)­145­5p expression was detected. Following H9c2 cell transfection with miR­145­5p mimics, the H9c2 cell viability, apoptosis, migration and invasion were also detected. Additionally, the target gene of miR­145­5p was assayed by Luciferase reporter assay. The protein expressions of Wnt­3a, Wnt5a, and ß­catenin in H9c2 cells under hypoxic conditions were also determined. The results revealed that hypoxia induced injury in H9c2 cells, including inhibiting cell viability, migration and invasion, and promoting cell apoptosis. Overexpression of TUG1 aggravated hypoxia­induced injury in H9c2 cells. In addition, miR­145­5p was negatively regulated by TUG1, and TUG1 overexpression aggravated hypoxia­induced injury via the downregulation of miR­145­5p. Furthermore, B­cell lymphoma 2 interacting protein 3 (Bnip3) was a target of miR­145­5p, and overexpression of Bnip3 aggravated hypoxia­induced cell injury by activating Wnt/ß­catenin signaling pathways in H9c2 cells. In conclusion, overexpression of TUG1 aggravated hypoxia­induced injury in cardiomyocytes by regulating the miR­145­5p­Binp3 axis. Activation of the Wnt/ß­catenin signaling pathway may be a key mechanism to mediate the role of TUG1 in regulating hypoxia­induced myocardial injury. TUG1 may be an effective diagnostic marker and therapeutic target for myocardial ischemia.