Ginsenoside Rg1 is a major active ingredient of Panax notoginseng radix which has demonstrated a number of pharmacological actions including a cardioprotective effect in vivo. This study investigated the protective effect and mechanism of ginsenoside Rg1 in cardiomyocytes hypoxia/reoxygenation (H/R) model. Pretreatment with ginsenoside Rg1 (60-120 microM) reduced lactate dehydrogenase release and increased cell viability in a dose-dependent manner. Fluorescence analysis demonstrated ginsenoside Rg1 reduced intracellular ROS and suppressed the intracellular [Ca(2+)] level. Cell lysate detected an increase of T-SOD, CAT, and GSH levels. The myocardial protection of ginsenoside Rg1 during H/R is partially due to its antioxidative effect and intracellular calcium homeostasis.
Karst rocky desertification is one of the major ecological and environmental problems that threaten the sustainable development of southwestern China. It is caused by irrational and intensive land-use patterns in karst geo-ecological environment. Therefore, it is vital to identify how human forces work on this degraded environment. Based on the soil erosion information in 2000 and remote sensing images of Guanling County collected in 2000 and 2007, four grades of karst rocky desertification data in 14 villages of Guanling County were extracted. Impacts of population, affluence, and other human forces on karst rocky desertification were analyzed using STIRPAT model. The results show that: 1) Factors of population and affluence had strong influence on karst rocky desertification. In the STIRPAT model analysis, the population and affluence coefficients were positive, indicating that the increase in population and affluence would lead to more serious desertification. 2) Factors of farmer correlated with karst rocky desertification negatively, especially the way of viewing the relationship between people and nature, and the level of knowledge about rocky desertification. Government behavior was not a significant factor in this analysis.3) The findings provide evidence that STIRPAT model can be used to analyze the relationship between human driving forces and rocky desertification.
Asthma is a common chronic respiratory disease. In a previous study, we found several circulating microRNA signatures associated with childhood asthma and selected miR-3162-3p for subsequent studies. Since the target proteins and underlying molecular mechanisms of miR-3162-3p in asthma etiopathogenesis are not well characterized, we designed this study to clarify its role. We employed bioinformatics and quantitative PCR methods as a first step to determine the target of miR-3162-3p, and we elucidated β-catenin. Luciferase assays and western blot analysis confirmed β-catenin as a direct target of miR-3162-3p as the 3’-untranslated region of β-catenin mRNA possesses a specific miR-3162-3p pairing site. The correlation between the expression levels of miR-3162-3p and β-catenin is confirmed by quantitative PCR and western blot studies in A549, Beas-2B and H1299 cell lines and OVA-induced asthma mouse model. Of note, upregulation of the endogenous miR-3162-3p level is concomitant with the reduction of β-catenin mRNA and protein expression levels. MiR-3162-3p antagomir treatment antagonizes the endogenous miR-3162-3p and effectively rescues the attenuation of endogenous β-catenin in OVA-induced asthmatic mice, which alleviates airway hyperresponsiveness and ameliorates airway inflammation. Collectively, our findings suggest a novel relationship between miR-3162-3p and β-catenin and clarify their mechanistic role in asthma etiopathogenesis.
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