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Elaeagnus angustifolia is one of the most extensively afforested tree species in environment-harsh regions of northern China. Despite its exceptional tolerance to saline soil, the intrinsic adaptive physiology has not been revealed. In this study, we investigated the growth, organ-level ionic relations and organic osmoregulation of the seedlings hydroponically treated with 0, 100 and 200 mM NaCl for 30 days. We found that the growth characteristics and the whole-plant dry weight were not obviously stunted, but instead, were even slightly stimulated by the treatment of 100 mM NaCl. In contrast, these traits were significantly inhibited by 200 mM NaCl treatment. Interestingly, as compared with the control (0 mM NaCl), both 100 and 200 mM NaCl treatments had a promotional effect on root growth as evidenced by 26.3% and 2.4% increases in root dry weight, respectively. Roots had the highest Na+ and Cl- concentrations and obviously served as the sink for the net increased Na+ and Cl-, while, stems might maintain the capacity of effective Na+ constraint, resulting in reduced Na+ transport to the leaves. K+, Ca2+ and Mg2+ concentrations in three plant organs of NaCl-treated seedlings presented a substantial decline, eventually leading to an enormously drop of K+/Na+ ratio. As the salt concentration increased, proline and soluble protein contents continuously exhibited a prominent and a relatively tardy accumulation, respectively, whereas soluble sugar firstly fell to a significant level and then regained to a level that is close to that of the control. Taken together, our results provided quantitative measures that revealed some robust adaptive physiological mechanisms underpinning E. angustifolia’s moderately high salt tolerance, and those mechanisms comprise scalable capacity for root Na+ and Cl- storage, effectively constrained transportation of Na+ from stems to leaves, root compensatory growth, as well as an immediate and prominent leaf proline accumulation.

Salinity is an important abiotic stress that severely depresses plant growth and development. Plants have evolved salinity tolerance mechanisms to enable adaptation to hostile environments. Generally, metabolic networks must be reconfigured to maintain metabolic homeostasis and to mitigate the stress. However, the mechanisms of plant stress-response systems are incompletely understood, which represents a bottleneck for further use of salinity-tolerant plants. Through its capability to provide both an overview and detailed analysis of changes in metabolic pathways, metabolomics has been widely applied to research plants’ stress resistance. In this study a metabolomics approach was adopted to describe changes in the metabolic profile of Nitraria tangutorum Bobr. suspension cells under salinity stress. Four salinity treatments (100, 150, 200, and 250 mM NaCl) were applied and liquid medium lacking NaCl was used as the control. After culture for 4 days, salinity stress affected the biomass, cell morphology, and osmotic potential of the suspension cells. Totals of 373 and 629 peaks were detected by gas chromatography/time-of-flight mass spectrometry in the aqueous phase and organic phase, respectively. Metabolic profiling differences were visualized by partial least squares-discriminant analysis models to highlight the changes in metabolic pathways under salinity stress. Twenty-six metabolites that showed differences in content were identified, including sugars, amino acids, and fatty acids. This research provides novel insights into the complex of metabolic pathways involved in the synthesis of stress-related metabolites, and of the salinity-tolerance mechanism in N. tangutorum suspension cells.

To observe the effect of oxidized low density lipoprotein (OxLDL) on arterial endothelial cells apoptosis in vivo, we established a model in which Sprague-Dawley rats were given intraperitoneal and intravenous injection of unmodified LDL (8 mg/kg every day) via the tail vein. Seven days after the injection, the aortic endothelial cells specimens were prepared by an en face preparation of rat aorta. The apoptotic cells were identified and counted by in situ nick and labelling (TUNEL) method and light microscopy. The numbers of the apoptotic cells were 12.52 +/- 4.71/field in the intraperitoneal injection control group, 11.41 +/- 2.94/field in the intravenous injection control group, 22.98 +/- 8.01/field in the intraperitoneal injection LDL group and 103.8 +/- 11.5/field in the intravenous injection LDL group, respectively. The difference was significant between injection LDL group and control (P0.01), and the difference was also significant between two LDL injection groups (P0.01). These findings suggest that injection of LDL can induce apoptosis in arterial endothelial cells and the effect is especially significant with intravenous injection LDL. After injection, oxidative modification of LDL may occur in local arteries and causes injury to the endothelial cells.

To investigate the expression of CD151 in human atherosclerosed artery and explore its clinical implications, Western blot and immunohistochemical techniques were used to determine the protein expression of CD151 in arterial tissues with atherosclerosis taken from 36 patients, including 26 cases who received bypass operation for peripheral artery atherosclerosis and 6 cases who died from coronary heart disease. The expression of CD151 in normal artery tissues from 15 healthy organ donators were also measured to serve as control. The results showed that expression of CD151 protein in atherosclerotic arteries was significantly higher than that in normal artery. In atherosclerotic arteries, CD151 expression was localized in vascular smooth muscle cells (VSMCs) in all tunica media and in partial subintima, while in normal artery, sparse expression was found in tunica media near adventitia. It is concluded that high CD151 protein expression in artery is associated with atherosclerosis and CD151 plays an important role in the atherosclerosis related to VSMC. The expression of CD151 in human atherosclerotic artery depends on the extent of atherosclerotic damage, it's independent of risk factors.

The effect of ginsenoside Rb1 on cardiomyocyte apoptosis after ischemia (30 min) and reperfusion (6 h) in rats was observed. The ischemia/reperfusion heart model was established by ligating left anterior descending branch of coronary artery in Wistar rats. The apoptotic cardiomyocytes were examined under transmission electron microscopy and counted by in situ nick end labeling (TUNEL) method and light microscopy. Results showed that (1) The apoptotic cardiomyocytes were found in ischemic regions in the ischemia/reperfusion group, but not in the sham-operating group under transmission electron microscopy; (2) The number of apoptotic cells were 134.45 +/- 45.61/field in the ischemia/reperfusion group, 0/field in the sham-operating group and 51.65 +/- 13.71/field in the ginsenoside Rb1-treated group. The differences were significant among the three groups (P0.01). It was concluded that myocardial ischemia-reperfusion could induce cardiomyocyte apoptosis, and ginsenoside Rb1 could significantly inhibit cardiomyocyte apoptosis induced by ischemia-reperfusion in rats, indicating that ginsenoside Rb1 could inhibit cardiomyocyte apoptosis induced by ischemia-reperfusion, thus alleviating ischemia-reperfusion injury.