LncRNA NRON alleviates atrial fibrosis through suppression of M1 macrophages activated by atrial myocytes.

The aim of the present study was to explore the role of long non-coding RNA (lncRNA) non-coding repressor of NFAT (NRON) in the atrial fibrosis and to explore whether its underlying mechanism was associated with macrophage polarization. Enzyme-linked immunosorbent assay (ELISA) analysis of pro-inflammatory cytokines revealed that NRON overexpression suppressed, whereas NRON silencing facilitated the angiotensin II (Ang II)-induced inflammatory response in primary cultured atrial myocytes. The chromatin immunoprecipitation (ChIP) results showed that nuclear factor of activated T cell 3 (NFATc3) was recruited to the promoter region of interleukin (IL) 12 (IL-12) in atrial myocytes. Further data showed that NRON overexpression suppressed, whereas NRON silencing further promoted the Ang II-induced NFATc3 nuclear transport and IL-12 expression in atrial myocytes. Moreover, RAW264.7 macrophages were incubated with the conditioned medium from the Ang II-treated atrial myocytes transfected with NRON and IL-12 overexpression vectors. IL-12 overexpression abrogated the NRON overexpression-mediated inhibition of RAW264.7 macrophage polarization to the M1-like phenotype. Additionally, mouse atrial fibroblasts were incubated with the culture medium from RAW264.7 macrophages treated as described above. IL-12 overexpression rescued the NRON overexpression-inhibited protein levels of fibrosis markers Collagen I/III in mouse atrial fibroblasts. Collectively, our data indicate that lncRNA NRON alleviates atrial fibrosis through suppression of M1 macrophages activated by atrial myocytes.

A novel method to prepare tussah/Bombyx mori silk fibroin-based films.

The possibility of using silk fibroin in biomaterials for tissue engineering is a subject of broad interest. In this study, Bombyx mori/tussah silk fibroin (BSF/TSF) blend films were prepared by solution casting using CaCl2/formic acid as a co-solvent and water as a rinse solvent. The morphology, crystallinity, thermal resistance, mechanical properties and water contact angle of the blend films as well as the biocompatibility were investigated. The BSF/TSF blend films displayed a smooth surface and specific nanostructure in their cross-section, originating from the nanofibril-preservation during fibroin dissolution. The water rinse process induced the formation of a stable ß-sheet structure. The BSF film showed superior mechanical properties to the TSF film, and the blending with TSF led to a significant reduction in the strength and elasticity of blend films. However, adding the TSF component could regulate the hydrophilic properties and enhance cell growth on the blend films. The BSF/TSF blend films with specific nanostructure, stable secondary structure, appropriate mechanical properties, and good biocompatibility, are promising candidates for application in regenerative medicine.

A novel effective chemical hemin for the treatment of acute carbon monoxide poisoning in mice.

There is no effective drug for the therapy of acute carbon monoxide (CO) poisoning. The purpose of the present study was to investigate the potential preventive and therapeutic effects of hemin on an animal model of acute CO poisoning and to provide a potential therapeutic candidate drug. A total of 80 Kunming mice were randomly divided into four groups, namely the air control, acute CO poisoning, hemin-treatment + CO and hemin-pretreatment + CO groups (n=20 each). Furthermore, the mortality rate of mice, blood carboxyhaemoglobin (HbCO) concentration and serum malondialdehyde (MDA) concentration were measured, and pathological changes of the hippocampal area were determined using histochemical staining. The mice with acute CO poisoning had a 50% mortality rate at 1 h, with an increase in blood HbCO, serum MDA levels and pathological impairments of the hippocampus. Furthermore, the mortality rate, blood HbCO and serum MDA levels of mice with pretreatment and treatment of hemin were decreased. Additionally, the pathological changes of the hippocampal area were improved in the hemin-treatment and hemin-pretreatment groups compared with the mice treated with CO. These results suggest that hemin is a novel effective chemical for the prevention and treatment of acute CO poisoning in mice. Therefore, the present study provides a novel method and experimental basis for the application of hemin in treating patients with acute CO poisoning.

Influence of levosimendan postconditioning on apoptosis of rat lung cells in a model of ischemia-reperfusion injury.

OBJECTIVE: To ascertain if levosimendan postconditioning can alleviate lung ischemia-reperfusion injury (LIRI) in rats. METHOD: One hundred rats were divided into five groups: Sham (sham), ischemia-reperfusion group (I/R group), ischemic postconditioning (IPO group), levosimendan postconditioning (Levo group) and combination postconditioning group of levosimendan and 5-Hydroxydecanoic acid (Levo+5-HD group). The apoptotic index (AI) of lung tissue cells was determined using the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Expression of active cysteine aspartate specific protease-3 ( active caspase-3), Bcl-2 and Bax in lung tissue was determined by immunohistochemical staining. The morphopathology of lung tissue was observed using light and electron microscopy. RESULTS: AI values and expression of active caspase-3, Bcl-2 and Bax of lung tissue in I/R and Levo+5-HD groups were significantly higher than those in the sham group ( P<0.05). AI values and expression of active caspase-3 and Bax were significantly lower, whereas that of Bcl-2 was higher significantly in the Levo group, compared with I/R and Levo+5-HD groups (P<0.05). Significant differences were not observed in comparisons between I/R and Levo+5-HD groups as well as IPO and Levo groups. CONCLUSION: LIRI can be alleviated by levosimendan, which simulates an IPO protective function. A postulated lung-protective mechanism of action could involve opening of mitochondrial adenosine triphosphate-sensitive potassium channels, relieving Ca2+ overload, upregulation of expression of Bcl-2, and downregulation of expression of active caspase-3 and Bax.