scholarly journals Silk fibroin/poly(L‑lactic acid‑co‑ε‑caprolactone) electrospun nanofibrous scaffolds exert a protective effect following myocardial infarction

2019 ◽  
Author(s):  
Mingjun Du ◽  
Jianmin Gu ◽  
Juan Wang ◽  
Yizheng Xue ◽  
Yiwen Ma ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Lactic Acid ◽  
Protective Effect ◽  
Silk Fibroin ◽  
Nanofibrous Scaffolds

scholarly journals Intermolecular interactions between B. mori silk fibroin and poly(l-lactic acid) in electrospun composite nanofibrous scaffolds

2017 ◽  
Vol 70 ◽  
pp. 777-787 ◽  
Author(s):  
Paola Taddei ◽  
Silvia Tozzi ◽  
Giampaolo Zuccheri ◽  
Simona Martinotti ◽  
Elia Ranzato ◽  
...  
Keyword(s):  
Lactic Acid ◽  
Intermolecular Interactions ◽  
Silk Fibroin ◽  
Nanofibrous Scaffolds

scholarly journals Protective effect of titanium tetrafluoride and silver diamine fluoride on radiation-induced dentin caries in vitro

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Beatriz Martines de Souza ◽  
Mayara Souza Silva ◽  
Aline Silva Braga ◽  
Patrícia Sanches Kerges Bueno ◽  
Paulo Sergio da Silva Santos ◽  
...  
Keyword(s):  
Lactic Acid ◽  
Protective Effect ◽  
Acid Production ◽  
Lactic Acid Production ◽  
Negative Control ◽  
Titanium Tetrafluoride ◽  
Silver Diamine Fluoride ◽  
Dentin Caries ◽  
Radiation Induced

AbstractThis in vitro study evaluated the protective effect of titanium tetrafluoride (TiF4) varnish and silver diamine fluoride (SDF) solution on the radiation-induced dentin caries. Bovine root dentin samples were irradiated (70 Gy) and treated as follows: (6 h): 4% TiF4 varnish; 5.42% NaF varnish; 30% SDF solution; placebo varnish; or untreated (negative control). Microcosm biofilm was produced from human dental biofilm (from patients with head-neck cancer) mixed with McBain saliva for the first 8 h. After 16 h and from day 2 to day 5, McBain saliva (0.2% sucrose) was replaced daily (37 °C, 5% CO2) (biological triplicate). Demineralization was quantified by transverse microradiography (TMR), while biofilm was analyzed by using viability, colony-forming units (CFU) counting and lactic acid production assays. The data were statistically analyzed by ANOVA (p < 0.05). TiF4 and SDF were able to reduce mineral loss compared to placebo and the negative control. TiF4 and SDF significantly reduced the biofilm viability compared to negative control. TiF4 significantly reduced the CFU count of total microorganism, while only SDF affected total streptococci and mutans streptococci counts. The varnishes induced a reduction in lactic acid production compared to the negative control. TiF4 and SDF may be good alternatives to control the development of radiation-induced dentin caries.

Fabrication and Characterization of Vitamin E TPGS Loaded Silk Fibroin/Hyaluronic Acid Nanofibrous Scaffolds

2013 ◽  
Vol 721 ◽  
pp. 274-277
Author(s):  
Li Li Ji ◽  
Qiao Ling Li ◽  
Zeng Hu Yang ◽  
Wei Jing Hu ◽  
Kui Hua Zhang
Keyword(s):  
Hyaluronic Acid ◽  
Vitamin E ◽  
Silk Fibroin ◽  
Ethanol Vapor ◽  
Random Coil ◽  
Burst Release ◽  
Nanofibrous Scaffolds ◽  
Vitamin E Tpgs ◽  
Polyethylene Glycol 1000 ◽  
Β Sheet

Vitamin E d-alpha-tocopheryl polyethylene glycol 1000 succinate (VE TPGS) loaded silk fibroin (SF)/ hyaluronic acid (HA) nanofibrous scaffolds were fabricated by means of electrospinning to biomimic the natural extracellular matrix. Scanning electronic microscopy (SEM) results indicated that electrospun VE TPGS loaded SF/HA nanofibers were ribbon-shaped, the width of nanofibers decreased slightly with the addition of VE TPGS to SF/HA blended solutions. Fourier transform infrared (FTIR) spectroscopy and Wide-angle X-ray diffraction (WAXD) curves revealed that VE TPGS did not induce SF conformation from random coil to β-sheet. SF conformation converted from random coil to β-sheet after being treated with 75% ethanol vapor. In vitro release studies confirmed VE TPGS had no obvious burst release and present good release behavior.

miR-187 modulates cardiomyocyte apoptosis and oxidative stress in myocardial infarction mice via negatively regulating DYRK2

2021 ◽  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Protective Effect ◽  
Myocardial Infarct ◽  
Annexin V ◽  
Cardiomyocyte Apoptosis ◽  
Ros Generation ◽  
Downstream Target

Myocardial infarction is a serious representation of cardiovescular disease, MicroRNAs play a role in modifying I/R injury and myocardial infarct remodeling. The present study therefore examined the potential role of miR-187 in cardiac I/R injury and its underlying mechanisms. miR-187 was inhibited or overexpressed in cardiomyocytes H/R models by pretreatment with miR-187 mimic or inhibitor to confirm the function of miR-187 in H/R. DYRK2 was inhibited or overexpressed in cardiomyocytes H/R models by pretreatment with DYRK2 inhibitor. A myocardium I/R mouse model was established. Circulating levels of miR-187 or DYRK2 was detected by quantitative realtime PCR and protein expression was detected by western blotting. The cell viability in all groups was determined by MTT assay and the apoptosis ratio was detected by flow cytometry after staining with Annexin V-FITC. The effect of miR-187 on cellular ROS generation was examined by DCFH-DA. The level of lipid peroxidation and SOD expression were determined by MDA and SOD assay. The findings indicated that miR-187 may be a possible regulator in the protective effect of H/R-induced cardiomyocyte apoptosis, cellular oxidative stress and leaded to DYRK2 suppression at a posttranscriptional level. Moreover, the improvement of miR-187 on H/R-induced cardiomyocyte injury contributed to the obstruction of DYRK2 expression. In addition, these results identified DYRK2 as the functional downstream target of miR-187 regulated myocardial infarction and oxidative stress.These present work provided the first insight into the function of miR-187 in successfully protect cardiomyocyte both in vivo and in vitro, and such a protective effect were mediated through the regulation of DYRK2 expression.

scholarly journals Diabetic Inhibition of Preconditioning- and Postconditioning-Mediated Myocardial Protection against Ischemia/Reperfusion Injury

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Xia Yin ◽  
Yang Zheng ◽  
Xujie Zhai ◽  
Xin Zhao ◽  
Lu Cai
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Protective Effect ◽  
Myocardial Protection ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Diabetic Patients ◽  
Protective Mechanisms ◽  
Gsk 3Β ◽  
Pathogenic Effects

Ischemic preconditioning (IPC) or postconditioning (Ipost) is proved to efficiently prevent ischemia/reperfusion injuries. Mortality of diabetic patients with acute myocardial infarction was found to be 2–6 folds higher than that of non-diabetic patients with same myocardial infarction, which may be in part due to diabetic inhibition of IPC- and Ipost-mediated protective mechanisms. Both IPC- and Ipost-mediated myocardial protection is predominantly mediated by stimulating PI3K/Akt and associated GSK-3β pathway while diabetes-mediated pathogenic effects are found to be mediated by inhibiting PI3K/Akt and associated GSK-3β pathway. Therefore, this review briefly introduced the general features of IPC- and Ipost-mediated myocardial protection and the general pathogenic effects of diabetes on the myocardium. We have collected experimental evidence that indicates the diabetic inhibition of IPC- and Ipost-mediated myocardial protection. Increasing evidence implies that diabetic inhibition of IPC- and Ipost-mediated myocardial protection may be mediated by inhibiting PI3K/Akt and associated GSK-3β pathway. Therefore any strategy to activate PI3K/Akt and associated GSK-3β pathway to release the diabetic inhibition of both IPC and Ipost-mediated myocardial protection may provide the protective effect against ischemia/reperfusion injuries.

scholarly journals Hyperlipidemia inhibits the protective effect of lisinopril after myocardial infarction via activation of dendritic cells

2020 ◽  
Vol 24 (7) ◽  
pp. 4082-4091
Author(s):  
Yuanji Ma ◽  
Leilei Ma ◽  
Jiaqi Ma ◽  
Runda Wu ◽  
Yunzeng Zou ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Dendritic Cells ◽  
Protective Effect
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