Sinomenine protects against atherosclerosis in apolipoprotein E-knockout mice by inhibiting of inflammatory pathway.

Atherosclerosis, a multifaceted and persistent inflammatory condition, significantly contributes to the progression of cardiocerebrovascular disorders, such as myocardial infarctions and cerebrovascular accidents. It involves the accumulation of cholesterol, fatty deposits, calcium and cellular debris in the walls of arteries, leading to the formation of plaques. Our aim is to investigate the potential of sinomenine to counteract atherosclerosis in mice lacking Apolipoprotein E (ApoE-/-) Mice. We employed the high-fat diet-induced method to induce atherosclerosis in ApoE-/- mice, and the mice were treated with sinomenine (5, 10, and 15 mg/kg) and simvastatin (0.5 mg/kg) for 12 weeks. Body weight, water intake, and food intake were assessed. Lipid parameters, oxidative stress, inflammatory cytokines, and mRNA levels were estimated. Sinomenine treatment remarkably (P < 0.001) suppressed body weight, along with food and water intake. Sinomenine altered the levels of total cholesterol (TC), high-density lipoprotein (HDL), triglyceride (TG), low-density lipoprotein (LDL), and very low-density lipoprotein (VLDL), which were modulated in the atherosclerosis group. Sinomenine treatment also altered the levels of oxidative stress parameters such as glutathione peroxidase (GPx), catalase (CAT), malonaldehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH). In addition, it modulated cardiac parameters like C-reactive protein (CRP), endothelin-1 (ET-1), thromboxane B2 (TXB2), nitric oxide (NO), cardiac troponin I (cTnI), lactate dehydrogenase (LDH), and creatinine kinase isoenzymes (CK-MB). Inflammatory cytokines interleukin (IL)-1α, IL-1ß, TNF-α, IL-6, and IL-10 were also affected. Sinomenine further suppressed the mRNA expression of IL-6, IL-17, IL-10, tumor necrosis factor-α (TNF-α), Il-1ß, monocyte chemoattractant protein-1 (MCP-1), MCP-2, MCP-3, transforming Growth Factor-1ß (TGF-1ß), vascular cell adhesion molecule 1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1). The results suggest that sinomenine remarkably suppressed the development of atherosclerosis in the early stage.

Correlation between Glycated Haemoglobin Level, Cardiac Function, and Prognosis in Patients with Diabetes Mellitus Combined with Myocardial Infarction.

Objective: This study was to investigate the correlation between glycated haemoglobin (HbA1c) level, cardiac function, and prognosis in patients with diabetes mellitus combined with myocardial infarction. Methods: Ninety-three patients with type 2 diabetes mellitus combined with acute myocardial infarction who were hospitalized and treated in our hospital from January 2021 to June 2021 were recruited for prospective analysis and equally divided into group A (HbA1c < 6.5%), group B (6.5% ≤ HbA1c ≤ 8.5%), and group C (HbA1c > 8.5%) using the random number table method, with 31 patients in each group. General data of patients were collected on admission and blood glucose and cardiac function indexes were measured; the incidence of myocardial infarction and death during the follow-up period was recorded at 6 months after discharge. Results: There was a significant difference in blood glucose (FBG) and HbA1c levels at fasting between the three groups (P < 0.05). There were statistically significant differences in plasma levels of N-terminal probrain natriuretic peptide (NT-proBNP) and uric acid (UA), left ventricular end diastolic diameter (LVEDD), left ventricular end systolic volume (LVESV), left ventricular ejection fraction (LVEF), and cardiac function classification of the New York Heart Association (NYHA) among the three groups (P < 0.05). By statistical analysis, the HbA1c level was positively correlated with FBG, NT-proBNP, UA, LVEDD, LVESD, and NYHA grades but negatively correlated with LVEF (P < 0.05). The incidence rate of myocardial infarction and mortality was significantly higher in group C than in groups A and B (P < 0.05). Conclusion: HbA1c level in patients with diabetes mellitus combined with myocardial infarction is closely related to the degree of cardiac function damage. Glycated haemoglobin levels are associated with the development of cardiac insufficiency in patients with acute myocardial infarction; glycated haemoglobin is also an independent predictor of major adverse cardiovascular events. Reasonable and effective blood glucose control is of great significance to the prognosis of patients.

Upregulation of FAM129B protects cardiomyocytes from hypoxia/reoxygenation-induced injury by inhibiting apoptosis, oxidative stress, and inflammatory response via enhancing Nrf2/ARE activation.

Family with sequence similarity 129, member B (FAM129B) has been identified as a novel cytoprotective protein that facilitates the survival of detrimentally stimulated cells. However, whether FAM129B is involved in regulating cardiomyocyte survival after myocardial ischemia-reperfusion injury is unknown. The goal of this work was to evaluate the potential role of FAM129B in regulating hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury in vitro. We demonstrated that exposure to H/R markedly downregulated the expression of FAM129B in cardiomyocytes. Functional experiments revealed that the upregulation of FAM129B improved H/R-exposed cardiomyocyte viability, and ameliorated H/R-induced cardiomyocyte apoptosis, the generation of reactive oxygen species (ROS), and pro-inflammatory cytokine release. The upregulation of FAM129B significantly increased the nuclear expression of nuclear factor-erythroid 2-related factor 2 (Nrf2), and reinforced Nrf2/antioxidant response element (ARE) activation in H/R-exposed cardiomyocytes. Moreover, FAM129B modulates Nrf2/ARE signaling in a Kelchlike ECH-associated protein 1-dependent manner. Notably, the inhibition of Nrf2 significantly blocked FAM129B-overexpression-induced cardioprotective effects in H/R-exposed cardiomyocytes. In summary, the findings of our work demonstrate that the upregulation of FAM129B ameliorates H/R-induced cardiomyocyte injury via enhancing Nrf2/ARE activation. Thus, our study indicates that FAM129B may play a role in myocardial ischemia-reperfusion injury and has the potential to be used as a cardioprotective target.

Plantamajoside protects H9c2 cells against hypoxia/reoxygenation-induced injury through regulating the akt/Nrf2/HO-1 and NF-κB signaling pathways.

Myocardial ischemia/reperfusion (I/R) injury has been found to be associated with oxidative stress. Plantamajoside (PMS) is a major compound of Plantago asiatica that was reported to possess cardioprotective and antioxidant effects. The current study was designed to investigate the effect of PMS on myocardial I/R injury. Rat cardiomyocytes H9c2 cells were exposed to hypoxia/reoxygenation (H/R) to establish in vitro model of myocardial I/R injury. MTT assay proved that H9c2 cells viability was significant reduced under H/R treatment, while the reduction was ameliorated by PMS. H/R-induced ROS production in H9c2 cells was suppressed by PMS. The decreased activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) in the H/R group were effectively elevated by PMS. In addition, treatment with PMS attenuated H/R-stimulated production of TNF-α, IL-6 and IL-1ß in H9c2 cells. Besides, PMS significantly suppressed bax expression and caspase 3 activity, as well as increased bcl-2 expression in H/R-stimulated H9c2 cells. Furthermore, we also found that PMS significantly enhanced the activation of Akt/Nrf2/HO-1 signaling pathway and suppressed the activation of NF-κB signaling pathway in H/R-stimulated H9c2 cells. These results provided substantial evidence that PMS protected against myocardial I/R injury via attenuating oxidative stress, inflammatory response and apoptosis. The protective effects of PMS were attributed to the Akt/Nrf2/HO-1 and NF-κB signaling pathways.

MiR-182-5p Mediated by Exosomes Derived From Bone Marrow Mesenchymal Stem Cell Attenuates Inflammatory Responses by Targeting TLR4 in a Mouse Model of Myocardial Infraction.

Exosomes derived from mesenchymal stem cells (MSCs) could protect against myocardial infarction (MI). TLR4 is reported to play an important role in MI, while microRNA-182-5p (miR-182-5p) negatively regulates TLR4 expression. Therefore, we hypothesize that MSCs-derived exosomes overexpressing miR-182-5p may have beneficial effects on MI. We generated bone marrow mesenchymal stem cells (BM-MSCs) and overexpressed miR-182-5p in these cells for exosome isolation. H2O2-stimulated neonatal mouse ventricle myocytes (NMVMs) and MI mouse model were employed, which were subjected to exosome treatment. The expression of inflammatory factors, heart function, and TLR4 signaling pathway activation were monitored. It was found that miR-182-5p decreased TLR4 expression in BM-MSCs and NMVMs. Administration of exosomes overexpressing miR-182-5p to H2O2-stimulated NMVMs enhanced cell viability and suppressed the expression of inflammatory cytokines. In addition, they promoted heart function, suppressed inflammatory responses, and de-activated TLR4/NF-κB signaling pathway in MI mice. In conclusion, miR-182-5p transferred by the exosomes derived from BM-MSCs protected against MI-induced impairments by targeting TLR4.

Astragaloside IV Ameliorates Myocardial Infarction Induced Apoptosis and Restores Cardiac Function.

BACKGROUND: Type 2 diabetes mellitus increases the risk of cardiovascular disease including myocardial infarction (MI). Inflammation and apoptosis have been implicated in the pathophysiology of MI. In the present study, the effects of astragaloside IV (AS-IV) on MI in diabetic mice were evaluated. METHODS: High glucose/high fat (HG/HF) and hypoxia culture condition were established to mimic diabetic condition. After administration of AS-IV to H9c2 myocytes, the cell apoptosis, viability, and activation of mitogen-activated protein kinase (MAPK) signaling pathways were detected. MI was induced in streptozotocin-induced diabetic mice. After administration of AS-IV to mice, cardiac function, cardiac fibrosis, inflammation, and activation of MAPK signaling pathway were detected. RESULTS: Astragaloside IV treatment significantly inhibited HG/HF and hypoxia-induced apoptosis of H9c2. AS-IV inhibited activation of JNK and p38 signaling pathway while promoting the activation of EKR signaling pathway. AS-IV treatment rescued cardiac function, suppressed cardiac fibrosis and inflammation, and differently regulated the activation of MAPK signaling pathways. CONCLUSION: Astragaloside IV prevented apoptosis and restored cardiac function in MI, which may be due to the regulation of MAPK signaling pathway in diabetes.

Genome-wide analysis of the mouse LIM gene family reveals its roles in regulating pathological cardiac hypertrophy.

LIM-domain proteins have been shown to be associated with heart development and diseases. Systematic studies of LIM family members at the genome-wide level, which are crucial to further understand their functions in cardiac hypertrophy, are currently lacking. Here, 70 LIM genes were identified and characterised in mice. The expression patterns of LIM genes differ greatly during cardiac development and in the case of hypertrophy. Both Crip2 and Xirp2 are differentially expressed in cardiac hypertrophy and during heart failure. In addition, the hypertrophic state of cardiomyocytes is controlled by the relative expression levels of Crip2 and Xirp2. This study provides a foundation for further understanding of the special roles of LIM proteins in mammalian cardiac development and hypertrophy.

Engineered macrophage membrane-enveloped nanomedicine for ameliorating myocardial infarction in a mouse model.

Myocardial infarction (MI) is the serious condition causing lots of death over the world. Myocytes apoptosis, inflammation, and fibrosis are three important factors implicated in pathogenesis of MI. Targeting these three factors has been shown to ameliorate MI and rescue cardiac function. Previous studies have demonstrated that microRNA (miR) 199a-3p protect against MI. In this study, we prepare macrophage membrane coated nanoparticles (MMNPs) containing miR199a-3p. We evaluate the effects of these NPs on apoptosis and cell proliferation in vitro and the effects on inflammation cytokine production, expression of fibrosis related proteins, cardiac injuries, and functions in MI mice. We find that the MMNPs have receptors of interleukin-1ß (IL-1ß), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-α) and can bind to these cytokines. MMNPs prevent hypoxia-induced apoptosis and promote cell proliferation, suppress the inflammation, and inhibit the cardiac fibrosis in MI mice. These results demonstrate that MMNPs ameliorate left ventricular remodeling and cardiac functions, and protect against MI, suggesting MMNPs containing miR199a-3p is a potential therapeutic approach to treat MI.

Upregulation of iASPP ameliorates hypoxia/reoxygenation-induced apoptosis and oxidative stress in cardiomyocytes by upregulating Nrf2 signaling.

The inhibitor of apoptosis-stimulating protein of p53 (iASPP) acts as a key modulator of cellular protection against oxidative stress. In the present work, we assessed the role of iASPP in the regulation of cardiomyocyte injury induced by hypoxia/reoxygenation (H/R). We found that H/R-exposed cardiomyocytes expressed decreased levels of iASPP. The upregulation of iASPP repressed H/R-induced injury by decreasing levels of apoptosis and reactive oxygen species production. The upregulation of iASPP increased nuclear factor (erythroid-derived 2)-like 2 (Nrf2) nuclear translocation and enhanced Nrf2 activation. The overexpression of Kelch-like ECH-associated protein 1 reversed iASPP-mediated promotion of Nrf2 activation. Nrf2 inhibition abrogated iASPP-mediated cardioprotective effects in H/R-exposed cardiomyocytes. Our work demonstrates that the upregulation of iASPP ameliorates H/R-induced apoptosis and oxidative stress in cardiomyocytes via potentiating Nrf2 signaling via modulation of Keap1.

E3-ubiquitin ligase TRIM6 aggravates myocardial ischemia/reperfusion injury via promoting STAT1-dependent cardiomyocyte apoptosis.

Cardiomyocyte apoptosis is a major cause of myocardial ischemia/reperfusion (MI/R) injury, in which the activation of the signal transducer and activator of transcription 1 (STAT1) plays an important role. The E3-ubiquitin ligase TRIM6 has been implicated in regulating STAT1 activity, however, whether it is associated with MI/R injury and the underlying mechanism are not determined. In this study, by investigating a mouse MI/R injury model, we show that TRIM6 expression is induced in mouse heart following MI/R injury. Additionally, TRIM6 depletion reduces and its overexpression increases myocardial infarct size, serum creatine phosphokinase (CPK) level and cardiomyocyte apoptosis in mice subjected to MI/R injury, indicating that TRIM6 functions to aggravate MI/R injury. Mechanistically, TRIM6 promotes IKKε-dependent STAT1 activation, and the inhibition of IKKε or STAT1 with the specific inhibitor, CAY10576 or fludarabine, abolishes TRIM6 effects on cardiomyocyte apoptosis and MI/R injury. Similarly, TRIM6 mutant lacking the ability to ubiquitinate IKKε and induce IKKε/STAT1 activation also fails to promote cardiomyocyte apoptosis and MI/R injury. Thus, these results suggest that TRIM6 aggravates MI/R injury through promoting IKKε/STAT1 activation-dependent cardiomyocyte apoptosis, and that TRIM6 might represent a novel therapeutic target for alleviating MI/R injury.

Irisin attenuates angiotensin II-induced cardiac fibrosis via Nrf2 mediated inhibition of ROS/ TGFß1/Smad2/3 signaling axis.

Angiotensin II-related cardiac fibrosis is one of the key pathological changes of the hypertrophied left ventricle in various heart disease. Irisin was recently reported to confer cardio-protective and anti-oxidative effects, while whether it can reverse the renin-angiotensin-aldosterone system(RAAS) activation related(angiotensin II-induced) cardiac fibrosis is unknown. In this study, we found that angiotensin II-induced cardiac dysfunction and fibrotic responses were dampened by irisin treatment in mice. Mechanistically, angiotensin II induced robust ROS generation, which in turn triggered activation of pro-fibrotic TGFß1-Smad2/3 signaling and subsequent collagen synthesis and fibroblast-myofibroblast transformation in cardiac fibroblasts. In contrast, Irisin treatment suppressed angiotensin II-induced ROS generation, TGFß1 activation, collagen synthesis and fibroblast-myofibroblast transformation, the effects of which was accompanied by Nrf2 activation and also abolished by a Nrf2 targeted siRNA. Taken together, we here identified irisin as a promising anti-fibrotic therapeutic for angiotensin II-related cardiac fibrosis.

Down-regulation of KIF2A inhibits gastric cancer cell invasion via suppressing MT1-MMP.

Gastric cancer accounts for a sizeable proportion of global cancer mortality with high morbidity and poor prognosis. Kinesin superfamily proteins (KIFs) are microtubule-dependent motor proteins that function as oncogenes in cancer cells, it has been discovered in recent years. Kinesin family member 2a (KIF2A), a member of the KIFs, has received attention for its role in carcinogenesis and its prognostic value in several human cancers such as breast cancer, colorectal cancer, and squamous cell carcinoma. However, the role of KIF2A in human gastric cancer remains unknown. In this study we aimed to explore the expression and biological functions of KIF2A in human gastric cancer cells, as well as to reveal its potential action mechanism. First, we found that KIF2A was markedly increased in gastric cancer cells (MKN-28, MKN-45, NCI-N87 and SGC-7901) compared to normal gastric mucosa epithelial cells (GES-1). Then KIF2A was successfully silenced in MKN-45 and SGC-7901 cells to facilitate further research into its function. We discovered that KIF2A silencing can significantly inhibit the growth and invasion of MKN-45 and SGC-7901 cells in a time-independent manner, accompanying a decreased expression of Membrane type 1-matrix metalloproteinase (MT1-MMP). When MT1-MMP was reintroduced into MKN-45 and SGC-7901 cells in the KIF2A-siRNA group, only invasion inhibition effects on MKN-45 and SGC-7901 cells induced by KIF2A silencing can be reversed. In conclusion, our study reveals that down-regulation of KIF2A can inhibit gastric cancer cell invasion by suppressing MT1-MMP.

Amelioration of myocardial ischemia-reperfusion injury by SIRT4 involves mitochondrial protection and reduced apoptosis.

Apoptosis and mitochondria dysfunction are key contributors to myocardial ischemia-reperfusion (MI-R) injury. SIRT4, a mitochondrial-localized sirtuin, controls cellular energy metabolism and stress response, and is abundantly present in the heart, however, its role in MI-R injury is not clear. In the current study, we demonstrate that SIRT4 is downregulated in cardiomyocytes both in vitro and in vivo models after MI-R. Functionally, SIRT4 overexpression decreases myocardial infarct size and serum creatine phosphokinase (CPK) level, and vice versa, SIRT4 depletion by siRNA increases myocardial infarct size and serum CPK level. Furthermore, we show that these protective roles of SIRT4 against MI-R injury are associated with preserved mitochondrial function and reduced myocardial apoptosis. Taken together, our findings indicate that SIRT4 ameliorates MI-R injury through regulating mitochondrial function and apoptosis, and suggest that manipulating SIRT4 may be of clinical benefit in MI-R injury.

Biocompatibility of quantum dots (CdSe/ZnS ) in human amniotic membrane-derived mesenchymal stem cells in vitro.

BACKGROUND AND AIM: Amniotic membrane-derived mesenchymal stem cells (hAM-dMSCs) are a potential source of mesenchymal stem cells which could be used to repair skin damage. The use of mesenchymal stem cells to repair skin damage requires safe, effective and biocompatible agents to evaluate the effectiveness of the result. Quantum dots (QDs) composed of CdSe/ZnS are semiconductor nanocrystals with broad excitation and narrow emission spectra, which have been considered as a new chemical and fluorescent substance for non-invasively labeling different cells in vitro and in vivo. This study investigated the cytotoxic effects of QDs on hAM-dMSCs at different times following labeling. METHODS: Using 0.75, 1.5 and 3.0 µL between quantum dots, labeled human amniotic mesenchymal stem cells were collected on days 1, 2 and 4 and observed morphological changes, performed an MTT cell growth assay and flow cytometry for mesenchymal stem cells molecular markers. RESULTS: Quantum dot concentration 0.75 µg/mL labeled under a fluorescence microscope, cell morphology was observed, The MTT assay showed cells in the proliferative phase. Flow cytometry expression CD29, CD31, CD34, CD44, CD90, CD105 and CD106. CONCLUSIONS: Within a certain range of concentrations between quantum dots labeled human amniotic mesenchymal stem cells has good biocompatibility.

A natural flavonoid glucoside icariin inhibits Th1 and Th17 cell differentiation and ameliorates experimental autoimmune encephalomyelitis.

Multiple sclerosis (MS) is an autoimmune disease that is characterized by recurrent episodes of T cell-mediated immune attack on central nervous system (CNS) myelin, leading to axon damage and progressive disability. Icariin, a natural flavonoid glucoside isolated from plants in the Epimedium family, has been proved to have various pharmacological activities. However, the effect of icariin on experimental autoimmune encephalomyelitis (EAE) has never been investigated. In our current study, we found that icariin treatment leads to alleviated inflammatory infiltration and reduced blood-brain barrier leakage (BBB) of the paracellular tracer (FITC-dextran) in EAE. Mice that received icariin-treated T cells also displayed lower EAE scores and better clinical recovery from EAE. Icariin administration suppresses the frequencies of Th1 and Th17 cells in the splenocytes and lymph node cells. Icariin-treated mice also show lower frequency of Th17 cells in CNS mononuclear cells. The effect of icariin on Th1 and Th17 cell differentiation may be mediated via modulation of dendritic cells (DCs). Furthermore, icariin suppresses the proliferation of T cells and the differentiation of Th1 and Th17 cells in vitro. In conclusion, icariin ameliorates EAE and this was associated with suppressed Th1 and Th17 cell differentiation.

Transplantation with cultured stem cells derived from the human amniotic membrane for corneal alkali burns: an experimental study.

Amniotic membranes (AM) have been used in a wide range of clinical applications. We successfully extracted mesenchymal stem cells (MSCs) from human AM, but little is known about the use and efficacy of human amniotic membrane-derived mesenchymal stem cells (hAM-dMSCs) for the treatment of alkali burns. We utilized hAM-dMSCs transplantation, AM grafting, and their combined use in the treatment of alkali burns. An experimental model in rabbits was devised to analyze the use of these techniques with immunocytochemistry and ELISA. The survival and migration of hAM-dMSCs labeled by SPION in the host were assessed with Prussian blue staining. Compared with the control group, the treated groups demonstrated faster reconstruction of the corneal epithelium, and lower levels of corneal opacification and neovascularization within corneal alkali burns. Furthermore, dark blue-stained particles were detected in the limbus corneae at day 28. These results demonstrated the ability of hAM-dMSCs to enhance epithelial healing and reduce corneal opacification and neovascularization in corneal alkali wounds.

Staining with methylthioninium chloride for the diagnosis of fungal keratitis.

The aim of this study was to investigate the potential efficacy of staining with methylthioninium chloride (MC) for the diagnosis of fungal keratitis. A total of 70 cases of fungal keratitis were included in the study from January 2009 to December 2010. The corneal scraping specimens of the patients were collected and stained with MC or a 10% potassium hydroxide (KOH)-based smear prior to microscopic examination. The staining results were confirmed with fungal culture and strain identification, which are recognized as 'gold standards' for the diagnosis of fungal keratitis. Among the 70 cases of fungal keratitis, 58 cases were positive and the positive rate was 82.86%. MC staining showed a positive rate of 62.86%, with higher levels of sensitivity (70.69%) and specificity (34.61%) compared with staining with the 10% KOH-based smear. The KOH-based smear showed a positive rate of 44.29% (P<0.05), a level of sensitivity of 44.83% (P<0.05) and a specificity of 17.95% (P<0.05). In addition, the MC staining showed false positive and negative rates of 25.00 and 29.31%, respectively, an accuracy index of 5.30% and positive and negative predictive values of 93.18 and 34.61%, respectively. The results indicate that MC staining is a fast and effective method for the early diagnosis of fungal keratitis.

Human amniotic membrane-derived mesenchymal stem cells labeled with superparamagnetic iron oxide nanoparticles: the effect on neuron-like differentiation in vitro.

Mesenchymal stem cells (MSCs) have the potential for self-renewal and multipotential differentiation to regenerate damaged tissues or recover functional absence in diseases. Superparamagnetic iron oxide nanoparticles (SPIONs) are used as contrast agents in magnetic resonance imaging (MRI) for labeling cells in vitro and for tracking SPION-labeled cells after transplantation in vivo. Human amniotic membrane-derived mesenchymal stem cells (hAM-dMSCs) have the capacity for neuron-like differentiation that could be used to cure central nervous system (CNS) diseases. The study investigated the impacts of cytotoxicity of SPIONs on neuron-like differentiation of hAM-dMSCs in both single (1×) and multiple (4×) SPIONs-labeled methods. hAM-dMSCs could be efficiently labeled at safe concentrations of SPIONs (≤14 µg/ml) without significantly affecting their viability (>80% after a MTT assay), special surface antigens (CD29, CD44, CD90, CD105 through flow cytometry), and neuron-like differentiation (nestin and neuron-specific enolase through immunocytochemistry and reverse transcription polymerase chain reaction). Compared with multiple (4×) SPION-labeled methods, a single (1×) SPION-labeled method avoided multiple SPION-labeled hAM-dMSCs and minimized the impact of cytotoxicity of SPIONs on neuron-like differentiation of hAM-dMSCs. Under safe concentrations of SPIONs, a single (1×) SPION-labeled method provided appropriate viability for SPIONs-labeled hAM-dMSCs and facilitated the MRI evaluation of hAM-dMSCs after transplantation.

[Treatment of brain injured rats through transplanting amniotic-derived mesenchymal stem cells in different ways].

OBJECTIVE: To compare the behavioral improvement to find the best transplantation approach for treating brain injury through transplanting amniotic-derived mesenchymal stem cells into brain injured rats in different ways. METHODS: Eighty brain injured Wista rats were randomly divided into a control group with brain injury alone (n=20) and a treatment group(n=60) which were further evenly divided into Group A (transplanted through the vena caudalis), Group B (transplanted through the ventriculus cerebri lateralis), and Group C (transplanted through the injured brain area). Each group was transplanted with amniotic-derived esenchymal stem cells, and their therapeutic efficacy would be evaluated through the neurological severity score (NSS). RESULTS: Compared with other groups, the behaviors of Group C had markedly improved. There was statistically significant difference in the 2 groups (P<0.05). Compared with the control group, the behaviors of Group A and Group B had marked improvement. There was statistically significant difference in the 3 groups (P<0.05). However, there was no significant difference between Group A and the control group (P>0.05). CONCLUSION: Transplanting the amniotic-derived mesenchymal stem cells into the injured brain area may be effective for brain injury in rats.