Impact of Intra-Aortic Balloon Counterpulsation on Prognosis of Patients with Acute Myocardial Infarction: A Meta-Analysis.

BACKGROUND: This study aimed to evaluate the impact of intra-aortic balloon counterpulsation (IABP) on the prognosis of patients with acute myocardial infarction (AMI). METHODS: We identified and included in this study AMI cases treated with IABP from January 1970 to May 2014. For statistical analysis, we utilized RevMan 5.0 software. RESULTS: Fourteen RCTs with a total population of 2538 were included in this study. The in-hospital and 30-day mortality rate in the IABP group was not significantly lower than those in the non-IABP group. Subgroup analysis according to the type of revascularization, OR values of TT subgroup, PCI subgroup, and CABG subgroup were 0.64 (95% CI 0.25-1.61, p = 0.34), 0.85 (95% CI 0.65-1.11, p = 0.23) and 0.46 (95% CI 0.13-1.63, p = 0.23). And OR values of AMI patients in the before and after PCI subgroup were 0.43 (95% CI 0.21-0.91, p = 0.03) and 1.36 (95% CI 0.76-2.41, p = 0.30). The 6-month mortality in the IABP group was not significantly lower than that in the non-IABP group. And OR values of 6-month mortalities of the before and after PCI subgroup were 0.47 (95% CI 0.26-0.86, p = 0.01) and 1.40 (95% CI 0.57-3.45, p = 0.47). CONCLUSIONS: IABP did not reduce the in-hospital and 30-day mortality of AMI patients, and did not reduce the 6-month mortality. But IABP used in AMI patients before PCI was associated not only with reduced in-hospital and 30-day mortality, but also reduced 6-month mortality.

Overexpression of tripartite motif containing 26 inhibits non-small cell lung cancer cell growth by suppressing PI3K/AKT signaling.

It has been reported that tripartite motif containing 26 (TRIM26) is involved in the tumorigenesis of some cancers, but its function in non-small cell lung cancer (NSCLC) is still unclear. In this study, we found that TRIM26 was markedly down-regulated in both of NSCLC tumor tissues and cell lines. Additionally, high expression of TRIM26 in NSCLC patients predicted a positive index for patients' overall survival. What is more, overexpression of TRIM26 significantly suppressed NSCLC cell growth. Our further studies indicated that overexpression of TRIM26 inhibited the phosphorylation of PI3K p85 and AKT. And overexpressed TRIM26 regulated cell cycle-related genes' expression, including downregulating CDK4, Cyclin A, Cyclin D1, Cyclin D3, and Cyclin E, and upregulating p27 expression. Finally, we found that TRIM26 up-regulated PTEN expression by stabilizing PTEN protein in NSCLC cells. Collectively, our present study indicated that TRIM26 was decreased in NSCLC and overexpression of TRIM26 inhibited NSCLC cell growth by suppressing PI3K/AKT pathway, which suggested that TRIM26 could be as a potential target for the treatment of NSCLC in the future.

Withaferin A attenuates ovalbumin induced airway inflammation.

The molecular mechanism of how airway inflammation develops is not fully understood. Withaferin A (WA) is a natural phytochemical isolated from the plant Withania somnifera. It is a well-investigated bioactive compound that possesses a variety of health-promoting effects, including anti-inflammatory and anti-oxidative activities. In the present study, the effect of WA on ovalbumin (OVA)-induced airway inflammation in mice was investigated. The results indicated that pre-treatment with WA inhibited OVA-induced lung injury and fibrosis progression in mice. Furthermore, WA significantly downregulated inflammatory cell infiltration into the bronchoalveolar lavage fluid and significantly reduced pro-inflammatory cytokine expression in the lung tissue specimens. Additionally, WA significantly suppressed transforming growth factor-b1 expression in lung tissues. WA also caused the downregulation of collagen I, collagen III, α-smooth muscle actin and tissue inhibitor of metalloproteinase-1, as well as SMADs and extracellular signal related kinase 1/2 inactivation. Notably, WA significantly reduced the activation of the NLRP3 inflammasome. The results indicate that WA may be an effective novel candidate for the treatment of airway inflammation.

Linarin prevents LPS­induced acute lung injury by suppressing oxidative stress and inflammation via inhibition of TXNIP/NLRP3 and NF­κB pathways.

Acute lung injury (ALI) is an important cause of morbidity and mortality for critically ill patients, and linarin (LR) may be a potential treatment for ALI as it reportedly has antioxidant, anti­inflammatory and apoptotic­regulating activity. In the present study, the authors report that saline and LR (12.5, 25 and 50 mg/kg) were applied to male C57BL/6 mice via gavage. Then, mice were intratracheally injected with either saline or lipopolysaccharide (LPS). LR­pretreatment attenuated LPS­induced ALI and platelet activation and reduced CD41 expression levels and neutrophil platelet aggregates. Additionally, LPS­triggered pulmonary myeloperoxidase activity and neutrophil infiltration in lung tissues, and this was eliminated by LR dose­dependently. Furthermore, LPS­induced oxidative stress and pro­inflammatory cytokine release were downregulated by LR by inhibiting thioredoxin­interacting protein and nuclear factor­κB signaling pathways, including their downstream and upstream signals, such as xanthine oxidase, NLR family WHAT, pyrin domain­containing 3 (NLRP3), apoptosis­associated speck­like protein containing a C­terminal caspase recruitment domain (ASC), caspase­1, IκB kinase­α (IKK­α) and IκBα. Moreover, in LPS­induced mice, the mitogen­activated protein kinase pathway was inactivated by LR. In vitro, LR reduced LPS­induced inflammation and oxidative stress, which was linked to reduction of ROS. In conclusion, LR pretreatment may be protective against LPS­induced ALI.