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Background:Myocardial ischemia-reperfusion injury (IRI) is an important injury mechanism of myocardial infarction. The purpose of this study was to explore the effects of L-carnitine (LC) on myocardial IRI and its mechanism. Material/Methods:The IRI model was made by ligating the left anterior descending coronary artery. Then, we injected LC intraperitoneally into the rats of the experimental group to assess the effect of LC on IRI rats by use of serum markers, Western blot, and qRT-PCR. H9c2 cells were cultured and then treated with hypoxia-reoxygenation. The effect of LC on oxidative stress, apoptosis, and nuclear transcription-related factor 2/heme oxygenase-1 (Nrf2/HO-1) signaling pathway of H9c2 cells were detected by Western blot, RT-PCR, and flow cytometry. Results:LC significantly reduced malondialdehyde (MDA), creatine kinase (CK), and lactate dehydrogenase (LDH) levels in rat myocardial tissue and increased superoxide dismutase (SOD) expression. LC also increased the expression of SOD1/2 and Bcl-2 in rat myocardial tissue and H9c2 cells and decreased the expression of caspase3/8 and Bax. In addition, LC increased the expression of Nrf2/HO-1 signaling pathway-related molecules in H9c2 cells and increased the activity of the Nrf2/HO-1 signaling pathway. Moreover, inhibition of the Nrf2/HO-1 signaling pathway attenuated the protective effect of LC on H9c2 cells. Conclusions:LC can activate the Nrf2/HO-1 signaling pathway and reduce oxidative stress and apoptosis in cardiomyocytes, thereby reducing myocardial IRI.

Imparting surface coatings with conductivity is an effective way to prevent fire and explosion caused by electrostatic discharge. TiO 2 is a commonly used paint; however, intrinsic TiO 2 has poor electrical conductivity. Herein, we develop a method to make TiO 2 coating highly conductive by doping Ca 2+ into the TiO 2 lattice based on the introduction of graphene. It is demonstrated that doping Ca 2+ increases the carrier density of TiO 2 and its morphology changes from a sphere to a spindle shape, which increases the interfacial contact area between TiO 2 and graphene. Therefore, resistivity can be greatly decreased due to the construction of fast charge transport pathways from TiO 2 to graphene, resulting from an increase in the speed of interfacial charge transfer. In addition, the electronic properties of the samples are also studied through first-principles calculations before and after Ca 2+ doping. The result of the theoretical analysis is in agreement with that of experiments. Thus, the lowest resistivity of Ca 2+ -TiO 2 /graphene can reach 0.004 Ω cm. Consequently, the feature of superior conductivity of the Ca 2+ -TiO 2 /graphene composite endows it with practical application potential in the field of antistatic coating.

Long non-coding RNAs (lncRNAs) are confirmed to be involved in modulating diabetic nephropathy (DN). The present study is aimed to explore the regulatory mechanism of lncRNA small nucleolar RNA host gene 15 (SNHG15) on pediatric DN. Human glomerular mesangial cells (HGMCs) were exposed to high glucose (HG) to produce an in vitro model. The results showed that SNHG15 was remarkably up-regulated in pediatric DN tissues and HG-induced HGMCs. Functional experiments indicated that both silencing of SNHG15 and overexpression of miR-141 elevated the cell viability, and suppressed the inflammation in HG-induced HGMCs. SNHG15 was identified to be a lncRNA that could bind to miR-141, and ICAM-1 was a downstream target gene of miR-141. Both the low expression of miR-141 and high expression of ICAM-1 reversed the inhibiting effect of SNHG15 knockdown on inflammatory response, and the promoting effect on cell viability. To conclude, our study revealed that silencing of SNHG15 ameliorated the malignant behaviors of pediatric DN via modulating the miR-141/ICAM-1 axis in vitro.