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Western blot analysis showed that OGD treatment induced TLR4, and NF-κB p65 subunit phosphorylation and caspase-1 upregulation, while co-culture with MSCs could reduce the effect of OGD treatment on endothelial cells. As expected, the effect of MSC-derived exosomes on OGD-treated endothelial cells was similar to that of MSCs. MSC-derived exosomes alleviated the OGD-induced decrease in the viability of endothelial cells, and increased levels of apoptosis, inflammatory factors, and the activation of inflammatory and inflammatory focal pathways. CONCLUSION Both MSCs and MSC-derived exosomes attenuated OGD-induced rat primary brain endothelial cell injury. These findings suggest that at least some of the protective effects of MSCs on endothelial cells are mediated by MSC-derived exosomes. Copyright© Bentham Science Publishers; For any queries, please email at [email protected] Adjuvants have been obtained empirically by trial and error experiments and today there is a tendency to rational design of adjuvants candidates, which will increasingly achieve effective and safe products. The aim of this work was to design and evaluate the compound IMR-23 derived from nitroimidazole as an immunomodulatory molecule. MATERIAL AND METHODS The IMR-23 molecule was obtained by a condensation reaction, cytotoxicity was tested by the sulforhodamine B assay. Adjuvanticity was evaluated in vivo and in vitro in J774A.1 cells and in the mouse model, respectively. RESULTS IMR-23 did not show cytotoxicity on HeLa, Vero cells and macrophages J774A.1, was able to induce the production of molecules involved in the inflammatory process, such as, cytokines and chemokines determined by ELISA, to induce the production of antibodies and to generate antigen-specific cells to ovalbumin and against the antigen GST-L1b. CONCLUSIONS These results open the possibility of further studies to obtain a proper balance of immunogenicity-toxicity in the use of IMR-23 as an adjuvant molecule. Copyright© Bentham Science Publishers; For any queries, please email at [email protected] Recently we developed a scalable scheme of synthesis of melphalan ester conjugate with 1,2-dioleoyl-sn-glycerol (MlphDG) and a protocol for the fabrication of its lyophilized liposomal formulation. OBJECTIVE Herein we compared this new convenient in use formulation of MlphDG with parent drug Alkeran® in rats with regard to a number of toxicological parameters and evaluated its antitumor efficacy in the model of breast cancer in mice. Selleck Taurochenodeoxycholic acid METHOD Liposomes of approximately 100 nm in diameter, consisting of egg phosphatidylcholine, soybean phosphatidylinositol, and MlphDG or placebo liposomes without drug were produced by extrusion and lyophilized. Alkeran® or liposomes recovered by addition of water were injected into the tail vein of animals. Clinical examination of rats consisted of detailed inspection of the behavior, general status, and hematological parameters. Mice with transplanted breast cancer WNT-1 were subjected to multiple treatment with the drugs; tumor growth inhibition was assessed, together with cellular immunity parameters. RESULTS Liposomes showed approximately 2 times lower acute toxicity and better tolerability than Alkeran® in terms of behavioral criteria. The toxic effects of liposomes on hemopoiesis were manifested at higher doses than in the case of Alkeran®, proportionally to the difference in LD50 values. The formulation inhibited tumor growth significantly more effectively than Alkeran®, delaying the start of the exponential growth phase and exhibiting no additional toxic effects toward bone marrow. CONCLUSION Lower toxicity of the liposomal formulation of MlphDG promises improved quality of life for cancer patients in need of treatment with melphalan. Presumably, list of indications for melphalan therapy could be extended. Copyright© Bentham Science Publishers; For any queries, please email at [email protected] Nanocarriers improve the efficacy of drugs by facilitating their specific delivery and protecting them from external environment resulting in a better performance against diseases. OBJECTIVE In this study, it was aimed to improve the efficacy of capecitabine against colorectal cancer by its entrapment in niosomes. Ether injection method was used to prepare niosomes composed of span 20 and cholesterol. METHODS Niosomes were evaluated by evaluating the entrapment efficiency, in-vitro drug release and cytotoxicity of capecitabine loaded niosomes. Niosomes were characterized by particle size analysis, transmission electron microscopy, Fourier transform infrared spectroscopy and differential scanning calorimetry for surface morphology and drug excipient interactions. RESULTS High encapsulation efficiency (90.55%) was observed which is anticipated to resolve the multi-drug resistance problem. Reported particle size was 180.9 + 5 nm with a negative zeta potential -21+0.5 mV and the kinetic study showed a concentration dependent release of the drug from the niosome. DSC study proved entrapment of the entire drug and its non-covalent bonding with the excipients. Cytotoxicity study of niosomes on CaCO2 cell line showed an improved IC50 value as compared to the free drug. CONCLUSION Enhanced cytotoxicity observed in the results further supports the suitability of niosome as a nanocarrier for pharmaceutical drug delivery. Copyright© Bentham Science Publishers; For any queries, please email at [email protected] of articular cartilage is an effective way to protect synovial joints from becoming osteoarthritic (OA) joints. Understanding of the molecular basis of articular cartilage degeneration will provide valuable information in the effort to develop cartilage preserving drugs. There are currently no disease-modifying OA drugs (DMOADs) available to prevent articular cartilage destruction during the development of OA. Current drug treatments for OA focus on the reduction of joint pain, swelling, and inflammation at advanced stages of the disease. However, based on discoveries from several independent research laboratories and our laboratory in the past 15 to 20 years, we believe that we have a functional molecular understanding of articular cartilage degeneration. In this review article, we present and discuss experimental evidence to demonstrate a sequential chain of the molecular events underlying articular cartilage degeneration, which consists of transforming growth factor beta 1, high-temperature requirement A1 (a serine protease), discoidin domain receptor 2 (a cell surface receptor tyrosine kinase for native fibrillar collagens), and matrix metalloproteinase 13 (an extracellular-matrix degrading enzyme).