The present study examined the relationship between personality traits and the response to acute psychological stress induced by a standardized laboratory stress induction procedure (the Trier Social Stress Test, TSST). The stress response was measured with a combination of cardiovascular reactivity, hypothalamic–pituitary–adrenal axis reactivity, and subjective affect (including positive affect, negative affect and subjective controllability) in healthy individuals. The Generalized Estimating Equations (GEE) approach was applied to account for the relationship between personality traits and stress responses. Results suggested that higher neuroticism predicted lower heart rate stress reactivity, lower cortisol stress response, more decline of positive affect and lower subjective controllability. Individuals higher in extraversion showed smaller cortisol activation to stress and less increase of negative affect. In addition, higher openness score was associated with lower cortisol stress response. These findings elucidate that neuroticism, extraversion and openness are important variables associated with the stress response and different dimensions of personality trait are associated with different aspects of the stress response.
The present study was designed to investigate the role of β‐amyloid (Aβ 1‐42 ) in inducing neuronal pyroptosis and its mechanism. Mice cortical neurons (MCNs) were used in this study, LPS + Nigericin was used to induce pyroptosis in MCNs (positive control group), and Aβ 1‐42 was used to interfere with MCNs. In addition, propidium iodide (PI) staining was used to examine cell permeability, lactate dehydrogenase (LDH) release assay was employed to detect cytotoxicity, immunofluorescence (IF) staining was used to investigate the expression level of the key protein GSDMD, Western blot was performed to detect the expression levels of key proteins, and enzyme‐linked immunosorbent assay (ELISA) was utilized to determine the expression levels of inflammatory factors in culture medium, including IL‐1β, IL‐18 and TNF‐α. Small interfering RNA (siRNA) was used to silence the mRNA expression of caspase‐1 and GSDMD, and Aβ 1‐42 was used to induce pyroptosis, followed by investigation of the role of caspase‐1‐mediated GSDMD cleavage in pyroptosis. In addition, necrosulfonamide (NSA), an inhibitor of GSDMD oligomerization, was used for pre‐treatment, and Aβ 1‐42 was subsequently used to observe the pyroptosis in MCNs. Finally, AAV9‐siRNA‐caspase‐1 was injected into the tail vein of APP/PS1 double transgenic mice (Alzheimer's disease mice) for caspase‐1 mRNA inhibition, followed by observation of behavioural changes in mice and measurement of the expression of inflammatory factors and pyroptosis‐related protein. As results, Aβ 1‐42 could induce pyroptosis in MCNs, increase cell permeability and enhance LDH release, which were similar to the LPS + Nigericin‐induced pyroptosis. Meanwhile, the expression levels of cellular GSDMD and p30‐GSDMD were up‐regulated, the levels of NLRP3 inflammasome and GSDMD‐cleaved protein caspase‐1 were up‐regulated, and the levels of inflammatory factors in the medium were also up‐regulated. siRNA intervention in caspase‐1 or GSDMD inhibited Aβ 1‐42 ‐induced pyroptosis, and NSA pre‐treatment also caused the similar inhibitory effects. The behavioural ability of Alzheimer's disease (AD) mice was relieved after the injection of AAV9‐siRNA‐caspase‐1, and the expression of pyroptosis‐related protein in the cortex and hippocampus was down‐regulated. In conclusion, Aβ 1‐42 could induce pyroptosis by GSDMD protein, and NLRP3‐caspase‐1 signalling was an important signal to mediate GSDMD cleavage, which plays an important role in Aβ 1‐42 ‐induced pyroptosis in neurons. Therefore, GSDMD is expected to be a novel therapeutic target for AD.
NADP-malic enzyme (NADP-ME, EC 22.214.171.124) functions in many different pathways in plants, and has recently been implicated in plant defense such as in responses to wounding and UV-B radiation. In this study, we isolated a complementary DNA (cDNA) clone by using the differential display method and screening of a root cDNA library of rice (Oryza sativa. L) under carbonate (NaHCO3) stress, and identified it as one of the rice NADP-ME genes (we named it NADP-ME2, GenBank accession no. AB053295). The 5' end of NADP-ME2 was obtained by the 5'-RACE method, and the full-length cDNA had a length of 2217 bp encoding 593 amino acids. Expression of NADP-ME2 mRNA in roots was induced by stress from carbonates (NaHCO3 and Na2CO3, NaCl, and environmental pH changes. NADP-ME2 transcripts increased during 72-h exposures to NaHCO3, NaCl, and PEG stresses. Furthermore, NADP-ME activities in leaves and roots of rice seedlings increased by more than 50% in the presence of carbonates (NaHCO3 and Na2CO3), NaCl, and PEG. These results indicate that rice NADP-ME2 responds to salts and osmotic stresses. Transgenic Arabidopsis plants over-expressing NADP-ME2 were obtained through transformation, screening, Northern analysis and in situ NADP-ME activity assay. Transgenic Arabidopsis plants over-expressing NADP-ME2 grew well in 1/2 x MS medium with 100 mM NaCl or 4% mannitol, whereas growth of wild-type (WT) Arabidopsis seedlings was strongly inhibited. In addition, under 125 mM NaCl stress, the root lengths of transgenic lines were about twice as long as those of the WT. These results suggest that NADP-ME2 has a role in enhancing tolerance of plants to salt and osmotic stress.
Increase of blood brain barrier (BBB) permeability after acute ischemia stroke is a predictor to intracerebral hemorrhage transformation (HT) for tissue plasminogen activator (tPA) thrombolysis and post-endovascular treatment. Previous studies showed that 2-h ischemia induced damage of BBB integrity and matrix metalloproteinase-2 (MMP-2) made major contribution to this disruption. A recent study showed that blocking β2-adrenergic receptor (β2-AR) alleviated ischemia-induced BBB injury by reducing hypoxia-inducible factor-1 alpha (HIF-1α) level. In this study, we sought to investigate the interaction of HIF-1α with MMP-2 and vascular endothelial growth factor (VEGF) in BBB injury after acute ischemia stroke. Rat suture middle cerebral artery occlusion (MCAO) model was used to mimic ischemia condition. Our results showed that ischemia produced BBB damage and MMP-2/9 upregulation was colocalized with Rhodamine-dextran leakage. Pretreatment with YC-1, a HIF-1α inhibitor, alleviated 2-h ischemia-induced BBB injury significantly accompanied by decrease of MMP-2 upregulation. In addition, YC-1 also prevented VEGF-induced BBB damage. Of note, VEGF was shown to be colocalized with neurons but not astrocytes. Taken together, BBB damage was reduced by inhibition of interaction of HIF-1α with MMP-2 and VEGF during acute cerebral ischemia. These findings provide mechanisms underlying BBB damage after acute ischemia stroke and may help reduce thrombolysis- and post-endovascular treatment-related cerebral hemorrhage.
The pathophysiology of idiopathic trigeminal neuralgia (ITN) has conventionally been thought to be induced by neurovascular compression theory. Recent structural brain imaging evidence has suggested an additional central component for ITN pathophysiology. However, far less attention has been given to investigations of the basis of abnormal resting-state brain activity in these patients. The objective of this study was to investigate local brain activity in patients with ITN and its correlation with clinical variables of pain. Resting-state functional magnetic resonance imaging data from 17 patients with ITN and 19 age- and sex-matched healthy controls were analyzed using regional homogeneity (ReHo) analysis, which is a data-driven approach used to measure the regional synchronization of spontaneous brain activity. Patients with ITN had decreased ReHo in the left amygdala, right parahippocampal gyrus, and left cerebellum and increased ReHo in the right inferior temporal gyrus, right thalamus, right inferior parietal lobule, and left postcentral gyrus (corrected). Furthermore, the increase in ReHo in the left precentral gyrus was positively correlated with visual analog scale (r=0.54; P=0.002). Our study found abnormal functional homogeneity of intrinsic brain activity in several regions in ITN, suggesting the maladaptivity of the process of daily pain attacks and a central role for the pathophysiology of ITN.
Expression of the gene (OsCA1) coding for carbonic anhydrase (CA) in leaves and roots of rice was induced by environmental stresses from salts (NaCl, NaHCO(3) and Na(2)CO(3)), and osmotic stress (10%, w/v, PEG 6000). CA activity of rice seedlings more than doubled under some of these stresses. Transgenic Arabidopsis over-expressing OsCA1 had a greater salt tolerance at the seedling stage than wild-type plants in 1/2 MS medium with 5 mM NaHCO(3), 50 mM NaCl, on 100 mM NaCl. Thus CA expression responds to environmental stresses and is related to stress tolerance in rice.
A metallothionein-like (rgMT) gene was isolated from a rice (Oryza sativa L.) root cDNA library that was prepared from plants grown under NaHCO3 stress. The rgMT gene expression was induced in rice leaves and roots under several abiotic stresses from salts (NaCl and NaHCO3), drought (PEG) and metals (CuCl2, ZnCl2, CdCl2). The results suggested that the rgMT gene was expressed in response to environmental stresses. The rgMT gene was expressed in Escherichia coli, and the final yield of the purified rgMT protein was 4.8 mg g(-1) dry cells. Tolerance of E. coli expressing GST-rgMT fusion protein to Cu2+, Zn2+ and Cd2+ was enhanced, and cells dry weight increased 0.04 mg, 0.17 mg and 0.07 mg in 1 ml culture treated with either CuCl2, ZnCl2 or CdCl2, respectively, compared with control after 6 h culture.
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