Zobrazení zdroje stránky Corbetthewitt0611

Moreover, the nanoparticles are proved to have superparamagnetic properties and fluorescence properties. In vitro cell experiments show that nanoparticles have excellent biocompatibility, blood compatibility and macrophage targeting. These results show that SDP-VCAM-1/Cur/Cy5.5 nanoparticles can be used not only as dual imaging probe for magnetic resonance (MR) and fluorescence imaging, but also as carriers to deliver chemotherapeutic drugs to inflammatory tissue, thus providing a promising opportunity for the treatment, molecular imaging and targeted therapy in atherosclerosis due to their established specificity and safety.<br /><br /> Bone marrow-derived mesenchymal stem cells (BMMSCs) exert cardioprotective effects on myocardial infarction (MI). In this investigation, we elucidated the protective effects of BMMSCs-exosomes (Exo) expressing microRNA-30e (miR-30e) against heart failure (HF) in MI rats.<br /><br /> First, the differentially expressed miRNAs were analyzed using a miRNA-based microarray of MI. Subsequently, we overexpressed miR-30e in rat BMMSCs to isolate exosomes. A rat model with MI was developed and treated with Exo. Next, we examined the cardiac function of the rats, followed by the myocardial tissue extraction. HE, TUNEL and Masson's staining were used to assess the protective effects of exosomes against HF in rats. Subsequently, H9C2 cells exposed to OGD were further co-cultured with Exo. We used bioinformatics to predict the target mRNA of miR-30e and verified the binding relationship. Finally, we tested the expression and role of NF-κB p65/Caspase-9 signaling in myocardial tissues and cells.<br /><br /> miR-30e was poorly expressed in myocardial tissues of MI rats. Moreover, treatment of rats with Exo overexpressing miR-30e ameliorated pathological damage, cardiomyocyte apoptosis, and fibrosis in rat myocardial tissues. Furthermore, miR-30e negatively regulated LOX1 expression, which was overexpressed in the MI rats, but further Exo treatment inhibited LOX1 expression. Moreover, Exo overexpressing miR-30e impaired the NF-κB p65/Caspase-9 signaling in myocardial tissues of MI rats. The NF-κB p65/Caspase-9 signaling inhibitor repressed the apoptosis and fibrosis of cardiomyocytes as well.<br /><br /> Exosomal miR-30e from rat BMMSCs markedly inhibited LOX1 expression, thereby downregulating the activity of the NF-κB p65/Caspase-9 signaling and ameliorating HF after MI in rats.<br /><br />Exosomal miR-30e from rat BMMSCs markedly inhibited LOX1 expression, thereby downregulating the activity of the NF-κB p65/Caspase-9 signaling and ameliorating HF after MI in rats.Reactive oxidative stress (ROS) related apoptosis in chondrocytes and extracellular matrix (ECM) degradation play crucial roles in the process of osteoarthritis. Prussian blue nanoparticles are known to scavenge ROS in cellular. Low-intensity pulsed ultrasound has been used as a non-invasive modality for the is widely used in clinical rehabilitation management of OA. In this study, we aim to investigate the effects of PBNPs/LIPUS combined treatment on knee osteoarthritis (KOA) and to determine whether phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling pathway mediates this process. Use LPS to process primary cells of knee joint cartilage to establish a cartilage knee arthritis model. After treated with LIPUS and PBNPs, cell viability was rated by CCK-8 and ROS levels were assessed by DCFH-DA. Articular pathological changes were observed by naked eyes, H&amp;E, and Safranin O staining, then monitored by cartilage lesion grades and Mankin's score. Cellular ROS, apoptosis rate, and TUNEL staining of chondrocytes were fairly decreased in the PBNPs group and the LIPUS group but drastically down-regulated in the PBNPs/LIPUS combination treatment group when compared with the LPS group. [https://www.selleckchem.com/products/imidazole-ketone-erastin.html Selleckchem Imidazole ketone erastin] Western blot results showed that the cleaved caspase-3, Bax, IL-1β, MMP3 and MMP13 in the PBNPs and LIPUS groups slightly decreased, and Bcl2 increased slightly, while in the combination treatment group, the former was significantly decreased, and Bcl2 was Significantly increased. The PBNPs/LIPUS combination treatment reduced cellular ROS, apoptosis, and matrix metalloproteinases (MMPs), as a consequence, alleviated articular cartilage damage in KOA. Moreover, the PBNPs/LIPUS combination treatment suppressed the JNK/c-Jun signal pathway.Hepatocellular carcinoma (HCC) is the leading cause of cancer-related deaths. Previous studies have suggested that mu-opioid receptor (MOR), a member of the opioid receptor family, is involved in the pathogenesis of HCC. However, the mechanism by which MOR regulates the biological behavior of HCC is still poorly understood. To address this problem, in this study, we investigated the role of MOR in the proliferation of HCC cell lines and the underlying mechanism. First, RT-PCR, western-blot and immunohistochemistry revealed higher expression of MOR in HCC cells and tissue than in non-tumor cells or adjacent tissue, and elevated expression of MOR was associated with jeopardized survival of HCC patients, as demonstrated by bioinformatic databases. Knockdown of MOR by specific siRNA attenuated the proliferation and migration of HCC cells and this effect could be reversed by rescue experiments, confirming the essential role of MOR in the proliferation of HCC. Moreover, results of colony formation assay, CCK8 test, flow cytometry and western blot suggested that a monoclonal antibody (mAb) specifically against MOR could inhibit proliferation of HepG2 and Huh7 cells via the MOR-CD147-p53-MAPK pathway, and the interaction between MOR and CD147 was verified by immunofluorescence colocalization and co-IP analysis. The mAb against MOR also enhanced the cisplatin-induced apoptosis of HCC cells by downregulating p-ERK, Bcl-2 and upregulating Bax. Taken together, these results suggest that MOR could regulate the proliferation of HCC cells in a CD147-p53-MAPK dependent manner. MOR possesses the potential to be a therapeutic target to treat HCC.With the development of regenerative medicine, various stem cells are increasingly considered for treating liver diseases. Various stem cells have been reported to play an essential role in liver recovery, and studies have verified the preliminary effectiveness and safety of these therapies. Stem cell-based therapies will emerge as an effective treatment strategy for liver diseases. Thus, the research progress and challenges to the related stem cells were reviewed, namely the classification of stem cells, cell culture, transplantation, cell tracing in the body, therapies for various liver diseases.