Synergistic protection of Schizandrin B and Glycyrrhizic acid against bleomycin-induced pulmonary fibrosis by inhibiting TGF-ß1/Smad2 pathways and overexpression of NOX4.

Pulmonary fibrosis, a progressive and lethal lung disease, is a major therapeutic challenge for which new therapeutic strategies are warranted. Schisandrin B (Sch B) and Glycyrrhizic acid (GA) are the principal active ingredients of Schisandra chinensis and Glycyrrhiza glabra respectively, which have been reported to protect against lung injures. The present study was aimed at exploring the combinatorial therapeutic effects on bleomycin-induced pulmonary fibrosis. Lung fibrotic injuries were induced in mice by a single intratracheal instillation of 5mg/kg bleomycin (BLM). Then, these mice were administered with Sch B (100mg/kg) or/and GA (75mg/kg) for 28days. BLM-triggered structure distortion, collagen overproduction, excessive inflammatory infiltration, pro-inflammatory cytokine release, and oxidative stress damages in lung tissues were attenuated to a higher degree by combinatorial treatment than by treatment of the individual agents. The expression of TGF-ß1 and the phosphorylation of its downstream target, Smad2 were enhanced by BLM, but weakened by Sch B or/and GA. Furthermore, the significant overexpression of NADPH oxidase 4 (NOX4) was observed in BLM-induced pulmonary fibrosis, which was inhibited by Sch B or/and GA. Our study reveals that the synergistic protection by Sch B and GA against BLM-induced pulmonary fibrosis is correlated to its anti-inflammatory, anti-oxidative and anti-fibrotic properties, involving inhibition of TGF-ß1/Smad2 signaling pathways and overexpression of NOX4.

[Response of leaf anatomical characteristics of Cyclobalanopsis gilva seedlings to drought stress].

In this study, the leaf anatomical characteristics and transpiration rate of one-year-old seedlings from three study areas including Qingyuan of Zhejiang Province, Dongkou and Jingzhou of Hunan Province were investigated using a pot planting experiment in which relative soil water content was kept as 75%-80% (control), 55%-60% (mild drought stress), 45%-50% (moderate drought stress), 30%-35% (severe drought stress), respectively. The results showed that drought stress significantly reduced the total thickness of the seedling leaves, the thickness of their upper and lower epidermis and the thickness of palisade tissue. The ratio of the palisade tissue to spongy tissue, stomatal length and width also decreased significantly, while the stomatal density increased significantly as the drought stress became more intense. The treatments of drought stress had no significant effect on the thickness of the main veins of the leaves although their xylem thickness varied depending on the seedlings from the different study sites. The change of leaf structure caused the change of physiological function. As drought stress was intensified, the transpiration rate of C. gilva seedlings decreased significantly. The ratio of the palisade tissue to spongy tissue, the thickness of the lower epidermis and stomatal density of the seedlings from Dongkou of Hunan Province were significantly greater, while the transpiration rate was significantly lower than those from other two study sites for all the drought stress treatments, implying that the C. gilva seedlings from Dongkou of Hunan Province had a stronger drought-resistance ability.

The effects and measures of auricular acupressure and interactive multimedia for smoking cessation in college students.

The earlier one starts to smoke, the more likely it is that one's tobacco use will increase. Either auricular acupressure or multimedia education could improve physiological health status and reduce smoking for young smokers. This study aimed to evaluate the effects of a 10-week auricular acupressure (AA) and interactive multimedia (IM) on smoking cessation in college smokers. A pre- and posttest control research design with two experiments (AA and IM) and one control was used. Thirty-two participants were in each of three groups. A significant difference from pretest to posttest among three groups was exhibited on carbon monoxide (CO), cotinine, and nicotine dependence. Scheffe's post hoc test found significances on CO in the AA between the IM and the control and cotinine and nicotine dependence between the AA and the control. After controlling the covariates, the main effect of the group was no difference in all outcomes. The interventions, especially AA, may contribute to a decrease of CO, cotinine, and nicotine dependence along with the time change. An analysis without controlling influences may overestimate interventional effects.

Pulmonary arterial hypertension and microRNAs--an ever-growing partnership.

Pulmonary arterial hypertension (PAH) is a debilitating condition with progressive remodeling of the pulmonary resistance vessels. PAH is characterized by multifocal, polyclonal lesions inhabited by cells that underwent phenotypic transition, resulting in altered cell proliferation and contractility, ultimately resulting in increased vascular resistance. Diagnosis of PAH is confounded by the fact that it is largely asymptomatic in the initial stages. In fact, idiopathic PAH patients >65 years of age cannot be diagnosed hemodynamically due to high pulmonary capillary wedge pressure. This highlights the need for defining more robust molecular biomarkers for PAH diagnosis and progression. Recent studies have indicated that microRNAs (miRNAs), a class of small noncoding RNAs that regulate gene expression, play a discrete role in vascular inflammation and in the etiology of cardiovascular pathologies inclusive of PAH and can potentially serve as diagnostic biomarkers. However, a cohesive understanding of global miRNA-mediated molecular events that control pulmonary vasculature plasticity is lacking which, if addressed systematically, can lead to detailed elucidation of the downstream cellular pathways that are affected by activation/silencing of silenced cognate transcripts. In turn, this can lead to not only robust biomarkers, but also to novel therapeutic strategies targeting more upstream regulators than the existing ones targeting more downstream effectors. The current review aims to provide a summary understanding of PAH, its associated pathophysiology, current knowledge of the role of miRNAs in PAH, and identifies grey areas that need further research for successful bench-to-bedside transition of these exciting new discoveries.