19 research outputs found

    Nanoceutical Adjuvants as Wound Healing Material: Precepts and Prospects

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    Dermal wound healing describes the progressive repair and recalcitrant mechanism of 12 damaged skin, and eventually, reformatting and reshaping the skin. Many probiotics, nutritional supplements, metal nanoparticles, composites, skin constructs, polymers, and so forth have been associated with the improved healing process of wounds. The exact mechanism of material-cellular interaction is a point of immense importance, particularly in pathological conditions such as diabetes. Bioengineered alternative agents will likely continue to dominate the outpatient and perioperative management of chronic, recalcitrant wounds as new products continue to cut costs and improve the wound healing process. This review article provides an update on the various remedies with confirmed wound healing activities of metal-based nanoceutical adjuvanted agents and also other nano-based counterparts from previous experiments conducted by various researchers

    Nuclear factor-kappa B and JNK mediate macrophage polarization shift induced by C-phycocyanin

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    381-389C-phycocyanin (C-pc), a fluorescent protein purified from the blue-green algae, Spirulina fusiformis, is reported to possess anti-inflammatory activity. Employing in vitro experiments and in vivo mouse models, we had earlier demonstrated the wound healing property of C-pc. In the current study, we evaluated the influence of C-pc on M1/M2 polarization of resting (M0) macrophages, using RAW 264.7 macrophage cells. Incubation of macrophages with C-pc resulted in upregulation of M1 markers (iNOS, IL-1β, IL-6 and TNF-α), and generation of reactive oxygen species and nitric oxide. In contrast, M2 markers, IL-10 and Arginase-1, exhibited reduced expressions. Immunoblotting and immunofluorescence studies revealed the activation and nuclear translocation of p65- NF-ĸB and JNK proteins. Inhibition studies showed that NF-ĸB and JNK were instrumental in shifting the polarization of M0 macrophages towards pro-inflammatory phenotype. NF-ĸB was responsible for the increase in TNF-α, IL-1β, and iNOS. JNK was responsible for the effect on IL-1β, IL-6 and Arg-1. This is the first report on the influence of NF-ĸB and JNK in mediating the pro-inflammatory action of C-pc, which could help towards phagocytosis and antimicrobial activity, processes required during the initial phases of wound healing. This study also exposes the biphasic action of C-pc towards modulating inflammatory processes

    Hemoglobin stimulates the expression of ADAMTS-5 and ADAMTS-9 by synovial cells: a possible cause of articular cartilage damage after intra-articular hemorrhage

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    Abstract Background ADAMTS (a disintegrin and metalloprotease with thrombospondin motifs) proteins play an important pathological role in matrix degeneration. Aggrecan degradation is a significant and critical event in early-stage osteoarthritis. To determine the effect of hemoglobin (Hb) on the ability of synovial tissues to produce ADAMTS family members, we examined the influence of Hb by synovial cells in an in vitro experimental system. Methods Synovial tissues were obtained from five young patients with meniscal injury under arthroscopic surgery. Primary cultures of human knee synovial cells were treated with different doses of human Hb (0, 25, 50, 100 μg/ml). The culture media were collected 24 h after Hb-treatment. In the time-course studies, cells were treated with and without 100 μg/ml Hb, and culture media were taken at 6, 12, and 24 h. To identify the proteins responsible for aggrecanase activity, Western blot analysis using antibodies against human ADAMTS-5, −8, −9, and −10; enzyme-linked immunosorbent assay (ELISA); and gene expression for ADAMTS-5 and -9 were examined. Statistical comparisons between each group were performed using paired t-tests. Results Western blot analysis revealed that Hb-treatment resulted in the expression of ADAMTS-5 and -9. Neither control group nor Hb-treated medium showed immunoreactivity against ADAMTS-8 or −10. In a dose-dependency study, the Hb-treated group showed significantly higher levels of ADAMTS-5 and -9 compared with the control (p < 0.05). There was no significant difference between 25, 50, and 100 μg/ml Hb-treated groups. In a time-course study, the ADAMTS-5 and -9 levels in the conditioned medium had significantly increased expression at 6, 12, and 24 h in the Hb-treated group (p < 0.05). Hb evoked significant expression of ADAMTS-9 mRNA at 12 and 24 h (p < 0.05). Conclusions These findings indicate that Hb induces the expression of ADAMTS-5 and -9 by synovial cells at low doses, even at an acute phase, and suggests a possible role for Hb in cartilage damage after intra-articular hemorrhage. The results also suggest a new potential therapeutic target by inhibiting the activities of ADAMTS-5 and -9 to prevent cartilage damage after intra-articular hemorrhage

    Peripheral neuropathy induced by drinking water contaminated with low-dose arsenic in Myanmar

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    Abstract Background More than 140 million people drink arsenic-contaminated groundwater. It is unknown how much arsenic exposure is necessary to cause neurological impairment. Here, we evaluate the relationship between neurological impairments and the arsenic concentration in drinking water (ACDW). Participants and methods A cross-sectional study design was employed. We performed medical examinations of 1867 residents in seven villages in the Thabaung township in Myanmar. Medical examinations consisted of interviews regarding subjective neurological symptoms and objective neurological examinations of sensory disturbances. For subjective neurological symptoms, we ascertained the presence or absence of defects in smell, vision, taste, and hearing; the feeling of weakness; and chronic numbness or pain. For objective sensory disturbances, we examined defects in pain sensation, vibration sensation, and two-point discrimination. We analyzed the relationship between the subjective symptoms, objective sensory disturbances, and ACDW. Results Residents with ACDW ≥ 10 parts per billion (ppb) had experienced a “feeling of weakness” and “chronic numbness or pain” significantly more often than those with ACDW  50 ppb). These data suggest a threshold for the occurrence of peripheral neuropathy due to arsenic exposure, and indicate that the arsenic concentration in drinking water should be less than 10 ppb to ensure human health
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