摘要 :
Due to its incomparable advantages, the application of transcriptome sequencing in the study of traditional Chinese medicine attracts more and more attention of researchers, which greatly promote the development of traditional Chi...
展开
Due to its incomparable advantages, the application of transcriptome sequencing in the study of traditional Chinese medicine attracts more and more attention of researchers, which greatly promote the development of traditional Chinese medicine. In this paper, the applications of transcriptome sequencing in traditional Chinese medicine were summarized by reviewing recent related papers.
收起
摘要 :
Background: Ventricular remodeling is a major pathological process of normal heart failure. With the aging of society, poor diet control, social, psychological and other risk factors in our country, the incidence of myocardial inf...
展开
Background: Ventricular remodeling is a major pathological process of normal heart failure. With the aging of society, poor diet control, social, psychological and other risk factors in our country, the incidence of myocardial infarction and hypertension is reported to increase yearly. Many treatment methods have effectively delayed the occurrence of ventricular remodeling. However, in order to prevent and delay the occurrence and development of ventricular remodeling, the new treatment strategy cannot be ignored.
收起
摘要 :
Neuroinflammation plays a critical role in the pathogenesis of ischemia/reperfusion (I/R) injury. Activated platelets are increasingly regarded as initiators and/or amplifiers of inflammatory processes in cerebral I/R injury. Salv...
展开
Neuroinflammation plays a critical role in the pathogenesis of ischemia/reperfusion (I/R) injury. Activated platelets are increasingly regarded as initiators and/or amplifiers of inflammatory processes in cerebral I/R injury. Salvianolic acid B (SAB) is the most abundant bioactive compound of Salviae miltiorrhizae, a well-known Chinese herb used to promote blood circulation and eliminating blood stasis. S. miltiorrhizae has been used clinically in Asia for the treatment of ischemic cerebrovascular diseases. In the present study, a rat model of transient middle cerebral artery occlusion (tMCAO) was established to investigate the neuroprotective effects and mechanisms of SAB treatment against focal cerebral I/R insult. The results showed that SAB treatment (3 mg/kg, 6 mg/kg and 12 mg/kg, i.p.) dose-dependently decreased I/R-induced neurological deficits at 24, 48, and 72 h after reperfusion and decreased plasma-soluble P-selectin and soluble CD40 ligand as early as 6 h after onset of I/12 insult. At 24 h after reperfusion, SAB treatment significantly reduced neuronal and DNA damage in the hippocampal CA1 region and decreased neural cell loss in the ischemic core. The I/R-induced pro-inflammatory mediator mRNA and protein overexpression in the penumbra cortex, including ICAM-1, IL-1 beta, IL-6, IL-8, and MCP-1, were significantly inhibited by SAB in a dose-dependent manner. Further studies suggested SAB treatment attenuated CD40 expression and NF-kappa B activation, which involved NF-kappa B/p65 phosphorylation and h kappa B alpha phosphorylation and degradation. In conclusion, our findings indicated that the neuroprotective effects of SAB post cerebral I/R injury are associated with the inhibition of both platelets activation and production of pro-inflammatory mediators and the downregulation of the CD40/NF-kappa B pathway. (C) 2017 Elsevier B.V. All rights reserved.
收起
摘要 :
To investigate the effects of formononetin on rats with gastric ulcer and further to explore its possible mechanism. Rats were randomly divided into sham operation group (Sham), model group (Model), omeprazole control group (Omepr...
展开
To investigate the effects of formononetin on rats with gastric ulcer and further to explore its possible mechanism. Rats were randomly divided into sham operation group (Sham), model group (Model), omeprazole control group (Omeprazole) and formononetin in different dose groups (FOR-L, FOR-M, FOR-H). Rats model with gastric ulcer were established by 100% glacial acetic acid. Hematoxylin-eosin (H&E) staining was used to observe the pathological morphology of gastric mucosa. Immunohistochemistry and enzyme-linked immunosorbent assay (ELISA) were used to detect the level of inflammatory and angiogenesis related factors. The expressions of nuclear factor kappa-B (NF-kappa B) signaling pathway-related proteins were detected by western blot. Formononetin and omeprazole could ameliorate the pathological morphology of gastric mucosa in gastric ulcer rats. Compared with Model group, the levels of tumor necrosis factor (TNF)-alpha, Interleukin (IL)-1 beta, IL-6, myeloperoxidase (MPO), human endothelin (ET)-1 and p-P65 protein in formononetin treatment and omeprazole groups were significantly decreased (p < 0.05). Moreover, formononetin could increase the content of vascular endothelial growth factor (VEGF), nitric oxide (NO) and the levels of CD34, tight junction proteins (ZO-1 and occludin) and p-I kappa B alpha in a dose-dependent manner. Formononetin can ameliorate gastric ulcer in rats by inhibiting inflammation and promoting gastric mucosal angiogenesis, and its mechanism maybe related to NF-kappa B signaling pathway.
收起
摘要 :
Mitochondria-derived peptides (MDPs) are a series of peptides encoded by mitochondrial DNA, and have similar functions to mitochondria. At present there are three types of MDPs that have been found, including Humanin, MOTS-c and S...
展开
Mitochondria-derived peptides (MDPs) are a series of peptides encoded by mitochondrial DNA, and have similar functions to mitochondria. At present there are three types of MDPs that have been found, including Humanin, MOTS-c and SHLP1-6. They are new metabolic regulators of human body, and play a cytoprotective role in maintaining mitochondrial function and cell viability under pressure. Increasingly researchers have demonstrated that MDPs have proved effects on cell survival, metabolism, response to stressors, and inflammation in vivo and vitro. Recently with the advance of research, it have shown that MDPs have significant effects on the development of cardiovascular diseases (CVD). In this review, we will cover the relationships of MDPs with cardiovascular risk factors, myocardial ischemia, reperfusion injury, myocardial fibrosis, and coronary microcirculatory dysfunction, and also their possible pathogenic mechanisms. MDPs are considered to be novel biomarkers or therapeutic targets for CVD.
收起
摘要 :
The objective of the present study was to develop the selection criteria of proton signals for the determination of scutellarin using quantitative nuclear magnetic resonance (qNMR), which is the main bioactive compound in brevisca...
展开
The objective of the present study was to develop the selection criteria of proton signals for the determination of scutellarin using quantitative nuclear magnetic resonance (qNMR), which is the main bioactive compound in breviscapine preparations for the treatment of cerebrovascular disease. The methyl singlet signal of 3-(trimethylsilyl)propionic-2,2,3,3-d(4) acid sodium salt was selected as the internal standard for quantification. The molar concentration of scutellarin was determined by employing different proton signals. To obtain optimum proton signals for the quantification, different combinations of proton signals were investigated according to two selection criteria: the recovery rate of qNMR method and quantitative results compared with those obtained with ultra-performance liquid chromatography. As a result, the chemical shift of H-2' and H-6' at delta 7.88 was demonstrated as the most suitable signal with excellent linearity range, precision, and recovery for determining scutellarin in breviscapine preparations from different manufacturers, batch numbers, and dosage forms. Hierarchical cluster analysis was employed to evaluate the determination results. The results demonstrated that the selection criteria of proton signals established in this work were reliable for the qNMR study of scutellarin in breviscapine preparations. Copyright (C) 2016, Food and Drug Administration, Taiwan. Published by Elsevier Taiwan LLC.
收起
摘要 :
The present study aimed to assess the protective effect of epigallocatechingallate (EGCG) against myocardial injury in a mouse model of heart failure and to determine the mechanism underlying regulation of the transforming growth ...
展开
The present study aimed to assess the protective effect of epigallocatechingallate (EGCG) against myocardial injury in a mouse model of heart failure and to determine the mechanism underlying regulation of the transforming growth factor-1/mothers against decapentaplegic homolog 3 (TGF-1/Smad3) signaling pathway. Mouse models of heart failure were established. Alterations in ejection fraction, left ventricular internal diastolic diameter (LVIDd) and left ventricular internal systolic diameter (LVIDs) were measured by echocardiography. Pathological alterations of myocardial tissue were determined by hematoxylin and eosin, and Masson staining. The levels of serum brain natriuretic peptide (BNP), N-terminal-proBNP, interleukin (IL)-1, IL-6, tumor necrosis factor-, malondialdehyde, superoxide dismutase and glutathione peroxidase were detected with ELISA. Expression of collagen I, collagen III were detected by western blotting and reverse transcription quantitative polymerase chain reaction. Transforming growth factor-1 (TGF-1), Smad3, phosphorylated (p)-Smad3, apoptosis regulator BAX (Bax), caspase-3 and apoptosis regulator Bcl(2) in mouse cardiac tissue were measured by western blotting. P-smad3 and TGF-1 were measured by immunofluorescence staining. EGCG reversed the alterations in LVIDd and LVIDs induced by establishment of the model of heart failure, increased ejection fraction, inhibited myocardial fibrosis, attenuated the oxidative stress, inflammatory and cardiomyocyte apoptosis and lowered the expression levels of collagen I and collagen III. Following treatment with TGF-1 inhibitor, the protective effect of EGCG against heart failure was attenuated. The results of the present study demonstrated that EGCG can inhibit the progression and development of heart failure in mice through inhibition of myocardial fibrosis and reduction of ventricular collagen remodeling. This protective effect of EGCG is likely mediated through inhibition of TGF-1/smad3 signaling pathway.
收起
摘要 :
Objective: To observe the effect of QiShenYiQi pill (QSYQ) on myocardial collagen metabolism in experimental autoimmune myocarditis rats, and to explore its mechanism of action.
摘要 :
TanshinoneIIA (TanIIA) has been demonstrated to possess numerous biological effects. However, the specific effect of TanIIA on macrophage polarization has not been reported. In this study, it was revealed that TanIIA might play a ...
展开
TanshinoneIIA (TanIIA) has been demonstrated to possess numerous biological effects. However, the specific effect of TanIIA on macrophage polarization has not been reported. In this study, it was revealed that TanIIA might play a pivotal role in macrophage polarization. As our results indicated, cell morphology was changed in RAW264.7 cells which were treated with LPS or LPS/TanIIA (0.1M, 1M, 10M). Subsequently, pro-inflammatory cytokine TNF- and anti-inflammatory cytokine IL-10 were measured by ELISA kits. Furthermore, TanIIA enhanced the expression of M2 macrophage markers (Arg1 and FIZZ1) and decreased the expression of markers associated with M1 macrophage polarization (iNOS and IL-1). Increased expression of CD206 was also detected by flow cytometry in TanIIA-treated groups. Mechanistically, it was revealed that TanIIA modulated macrophage polarization by ameliorating mitochondrial function and regulating TLR4-HMGB1/CEBP- pathway. In addition, increased expression of miR-155 was observed in RAW264.7 cells incubated with LPS and were effectively inhibited by TanIIA. Taken together, it was suggested that TanIIA inhibits inflammatory response and promotes macrophage polarization toward an M2 phenotype, which provides new evidence for the anti-inflammation activity of TanIIA.
收起
摘要 :
Curcumin is a key polyphenolic curcuminoid extracted from the root of turmeric rhizome Curcuma longa Linn, which is a frequently used Chinese herb for the treatment of cancer. The aim of the present study was to investigate the me...
展开
Curcumin is a key polyphenolic curcuminoid extracted from the root of turmeric rhizome Curcuma longa Linn, which is a frequently used Chinese herb for the treatment of cancer. The aim of the present study was to investigate the mechanism of the inhibitory effects of curcumin on nude mice with lung cancer A549 cell subsets side population (SP) and non-SP (NSP) cells. BALB/c mice were subcutaneously injected with the tumor cells of A549 SP or NSP subsets consisting of 1x10(9) cells/l (0.2 ml in total). After 16 days of inoculation with A549, the mice were intraperitoneally injected with curcumin (100 mg/kg, 0.2 ml) once every other day, eight times in total. A series of assays were performed to detect the effects of curcumin on: i) Tumor weight and size; ii) Notch and hypoxia inducible factor 1 (HIF-1) mRNA expression by quantitative polymerase chain reaction; and iii) vascular endothelial growth factor (VEGF) and nuclear factor-kappa B (NF-kappa B) by immunohistochemistry. It was determined that curcumin decreased the tumor weight and size, downregulated the expression of Notch and HIF-1 mRNA and suppressed the VEGF and NF-kappa B expression. These results indicated that curcumin inhibited lung cancer growth through the regulation of angiogenesis mediated by VEGF signaling.
收起
原文获取