Chronic obstructive pulmonary disease (COPD) is a pathological inflammatory condition of the lungs that is associated with high rates of mortality. Although long non-coding RNAs (lncRNAs) serve a role in lung diseases, their functions in COPD pathogenesis are relatively unknown. The present study aimed to assess the role of differentially expressed lncRNAs in COPD.  https://www.selleckchem.com/products/Acadesine.html  Expression profile analysis of six lncRNAs in age-matched COPD and non-COPD tissues were conducted. Among the six tested lncRNAs, metastasis-associated in lung adenocarcinoma transcript 1 (MALAT1) was the most consistently overexpressed in COPD lung tissue specimens. To model COPD in vitro, human lung fibroblasts were treated with transforming growth factor-β (TGF-β) and MALAT1 was knocked down by small interfering RNA. This promoted cell viability and concurrently inhibited the expression of mesenchymal proteins, fibronectin and α-smooth muscle actin. In COPD, cell senescence is linked to the activation of mammalian target of rapamycin complex 1 (mTORC1). Upon gene silencing of MALAT1 in non-TGF-β-treated cells, cells demonstrated constitutive activation of mTORC1, which was assessed by the protein expression levels of mTORC1 substrate S6 kinase (S6K1). By contrast, upon MALAT1 silencing in the TGF-β-treated cells, mTORC1 activation was not suppressed, despite the mesenchymal cell markers protein expression levels being downregulated. Thus, lncRNA MALAT1 may represent a potent biomarker in COPD patients and may act as a target for both diagnostic and therapeutic purposes.In the present study, the ability of baicalin to relieve neuropathic pain due to spinal nerve ligation in rats was explored, and the relationship between baicalin and α2-adrenoceptors (α2-AR) was determined. The neuropathic pain model was established by ligating the L5-L6 spinal nerves in Sprague-Dawley rats. Several α2-AR antagonists were injected into the intramedullary sheath to evaluate the role of baicalin in neuropathic pain. The antagonists included nonselective α2-AR antagonist idazoxan, α2a-AR antagonist BRL 44408, α2b-AR antagonist ARC 239 and α2c-AR antagonist JP 1302. The rats were divided into an untreated control group, saline group, baicalin group and baicalin + α2-AR antagonist groups. Paw withdrawal threshold (PWT) was tested to assess the level of pain felt by the rats. The levels of α2-AR mRNA were tested by reverse transcription-quantitative PCR. Inflammatory factors, including tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-17 and IL-1β, were analyzed by ELISA. The histopathological. In conclusion, intrathecal injection of baicalin produced an antiallodynic effect in a spinal nerve ligation-induced neuropathic pain model. The mechanism may be related to the regulation of a2-AR expression.Liver injury occurs frequently during sepsis, which leads to high mortality and morbidity. A previous study has suggested that salvianolic acid B (SalB) is protective against sepsis-induced lung injury. However, whether SalB is able to protect against sepsis-induced liver injury remains unclear. The present study aimed to investigate the effects of SalB on sepsis-induced liver injury and its potential underlying mechanisms. Sepsis was induced in mice using a cecal ligation and puncture (CLP) method. The mice were treated with SalB (30 mg/kg intraperitoneally) at 0.5, 2 and 8 h after CLP induction. Pathological alterations of the liver were assessed using hematoxylin and eosin staining. The serum levels of alanine transaminase (ALT), aspartate aminotransferase (AST), tumor necrosis factor (TNF)-α and interleukin (IL)-6 were measured. The hepatic mRNA levels of TNF-α, IL-6, Bax and Bcl-2 were also detected. The results suggested that treatment with SalB ameliorated sepsis-induced liver injury in the mice, as supported by the mitigated pathologic changes and lowered serum aminotransferase levels. SalB also decreased the levels of the inflammatory cytokines TNF-α and IL-6 in the serum and the liver of the CLP model mice. In addition, SalB significantly downregulated Bax expression and upregulated Bcl-2 expression, and upregulated the expression levels of SIRT1 and PGC-1α. However, when sirtuin 1 (SIRT1) small interfering RNA was co-administered with SalB, the protective effects of SalB were attenuated and the expression levels of SIRT1 and PGC-1α were reduced. In summary, these results indicate that SalB mitigates sepsis-induced liver injury via reduction of the inflammatory response and hepatic apoptosis, and the underlying mechanism may be associated with the activation of SIRT1/PGC-1α signaling.The present study aimed to investigate changes in the levels of metabolites and appetite control factors caused by different dietary interventions in Sprague Dawley (SD) rats. A total of 35 male SD rats were weaned and immediately randomly assigned to five groups. The control group was given ad libitum access to a normal chow diet, and the other groups received a high-fat diet (FAT group), high-sugar diet, high-fibre or high-protein diet (PRO group) for 4 weeks. The high-fat diet contributed to weight gain and adipose tissue formation, and affected lipid indexed. The FAT group had a higher body weight, Lee's index, adipose mass and glucose tolerance than all of the other groups. The opposite effect was observed in the PRO group. High-performance liquid chromatography revealed that short-chain fatty acid and amino acid formation were affected by the various diets. In addition, differences in the mRNA expression levels of leptin, ghrelin and associated receptors were determined in the gastrointestinal, adipose and hypothalamus tissues. The present study provides further evidence of the role of diet in obesity development and prevention. It also highlights the role of intestinal metabolites and appetite control factor expression in the pathogenesis of obesity in SD rats.Patients with hepatitis B virus (HBV)-related acute-on-chronic liver failure (ACLF) exhibit complex hemostatic defects. Thromboelastography (TEG) can be used to reveal global hemostasis in patients with liver disease; however, little is known about the association between TEG and the outcome of patients with HBV-related ACLF. The present study aimed to investigate the value of TEG for predicting 90 day mortality in patients with HBV-related ACLF. A total of 51 patients with HBV-related ACLF, 26 patients with chronic hepatitis B (CHB) and 26 healthy controls (HC) were enrolled in the present study. TEG, standard coagulation tests, routine blood tests, biochemical markers and demographic variables were recorded and assessed for prognostic value. The results indicated that a prolonged reaction and kinetics (K) time, a shortened α angle and a decreased maximum amplitude (MA) and coagulation index (CI) were observed in patients with HBV-related ACLF, compared with CHB and HC subjects. Patients with HBV-related ACLF in the mortality group exhibited a decrease in α angle, MA, lysis at 30 min, CI, fibrinogen and platelet count, and an increase in K time, international normalized ratio (INR) and the model for end-stage liver disease (MELD) score in comparison with the survival group.