Argon Plasma Jet-Treated Poly (Vinyl Alcohol)/Chitosan and PEG 400 Plus Mangifera indica Leaf Extract for Electrospun Nanofiber Membranes: In Vitro Study.

The wound-healing process can be disrupted at any stage due to various internal and external factors. The inflammatory stage of the process plays a vital role in determining the outcome of the wound. Prolonged inflammation due to bacterial infection can lead to tissue damage, slow healing, and complications. Wound dressings made using materials such as poly (vinyl alcohol) (PVA), chitosan (CS), and poly (ethylene glycol) (PEG) with Mangifera extract (ME) added can help reduce infection and inflammation, creating a conducive environment for faster healing. However, creating the electrospun membrane is challenging due to balancing various forces such as rheological behavior, conductivity, and surface tension. To improve the electrospinnability of the polymer solution, an atmospheric pressure plasma jet can induce chemistry in the solution and increase the polarity of the solvent. Thus, this research aims to investigate the effect of plasma treatment on PVA, CS, and PEG polymer solutions and fabricate ME wound dressing via electrospinning. The results indicated that increasing plasma treatment time increased the viscosity of the polymer solution, from 269 mPa∙to 331 mPa∙s after 60 min, and led to an increase in conductivity from 298 mS/cm to 330 mS/cm and an increase in nanofiber diameter from 90 ± 40 nm to 109 ± 49 nm. Incorporating 1% mangiferin extract into an electrospun nanofiber membrane has been found to increase the inhibition rates of Escherichia coli and Staphylococcus aureus by 29.2% and 61.2%, respectively. Additionally, the fiber diameter decreases when compared with the electrospun nanofiber membrane without ME. Our findings demonstrate that electrospun nanofiber membrane with ME has anti-infective properties and can promote faster wound healing.

A compact pulse-modulation cold air plasma jet for the inactivation of chronic wound bacteria: development and characterization.

A compact low-temperature plasma jet device was developed to use ambient air as plasma gas. The device was driven by a 2.52-kV high-voltage direct-current pulse in a burst mode, with a repetition rate of 2 kHz. The maximum plasma discharge current was 3.5 A, with an approximately 10 ns full-width half-maximum. Nitric oxide, hydroxyl radical, atomic oxygen, ozone, and hydrogen peroxide-important reactive oxygen and nitrogen species (RONS)-were mainly produced. The amount of plasma-generated RONS can be controlled by varying the pulse-modulation factors. After optimization, the plasma plume length was approximately 5 mm and the treatment temperature was less than 40 °C. The preliminary bactericidal effects were tested on Staphylococcus aureus, Pseudomonas aeruginosa, and methicillin-resistant S. aureus (MRSA), and their biofilms. The results showed that the plasma can effectively inactivate S. aureus, P. aeruginosa, and MRSA in both time- and pulse-dependent manner. Thus, this produced plasma device proved to be an efficient tool for inactivating deteriorating bacteria. Further versatile utilization of this portable plasma generator is also promising.

LL-37 alone and in combination with IL17A enhances proinflammatory cytokine expression in parallel with hyaluronan metabolism in human synovial sarcoma cell line SW982-A step toward understanding the development of inflammatory arthritis.

LL-37 is the only human cathelicidin-family host defense peptide and has been reported to interact with invading pathogens causing inflammation at various body sites. Recent studies showed high levels of LL-37 in the synovial-lining membrane of patients with rheumatoid arthritis, a common type of inflammatory arthritis. The present study aims to investigate the role of LL-37 on mechanisms associated with pathogenesis of inflammatory arthritis. The effects of LL-37 on the expression of proinflammatory cytokines, hyaluronan (HA) metabolism-related genes, cell death-related pathways, and cell invasion were investigated in SW982, a human synovial sarcoma cell line. Time-course measurements of proinflammatory cytokines and mediators showed that LL-37 significantly induced IL6 and IL17A mRNA levels at early time points (3-6 hr). HA-metabolism-related genes (i.e., HA synthase 2 (HAS2), HAS3, hyaluronidase 1 (HYAL1), HYAL2, and CD44) were co-expressed in parallel. In combination, LL-37 and IL17A significantly enhanced PTGS2, TNF, and HAS3 gene expression concomitantly with the elevation of their respective products, PGE2, TNF, and HA. Cell invasion rates and FN1 gene expression were also significantly enhanced. However, LL-37 alone or combined with IL17A did not affect cell mortality or cell cycle. Treatment of SW982 cells with both LL-37 and IL17A significantly enhanced IKK and p65 phosphorylation. These findings suggest that the chronic production of a high level of LL-37 may synchronize with its downstream proinflammatory cytokines, especially IL17A, contributing to the co-operative enhancement of pathogenesis mechanisms of inflammatory arthritis, such as high production of proinflammatory cytokines and mediators together with the activation of HA-metabolism-associated genes and cell invasion.

Ethanolic extract of Kaempferia parviflora interrupts the mechanisms-associated rheumatoid arthritis in SW982 culture model via p38/STAT1 and STAT3 pathways.

BACKGROUND: Kaempferia parviflora Wall. ex Baker (KP) has long been used in traditional medicine to treat various diseases because active compounds in rhizome extracts are important anti-inflammatory agents. PURPOSE: This study aims to investigate the effects of an ethanolic extract of KP on the molecular mechanisms associated with rheumatoid arthritis (RA), which was induced by a combination of proinflammatory cytokines (IL-1ß or TNF-α with IL-17A) in a human synovial sarcoma cell line (SW982) culture model. METHODS: SW982 cells pretreated with cytokines were incubated with KP extract at 3-30 µg/ml, or three major compounds of KP (5,7-dimethoxyflavone, 5,7,4'-trimethoxyflavone, and 3,5,7,3',4'-pentamethoxyflavone) for up to 72 h. Dexamethasone was used as positive control. RA-associated genes and inflammatory products were measured in parallel with cell death genes. Apoptosis by flow cytometry and migration assay were also analyzed. Western blotting was used to examine the effects on intracellular signaling mechanisms. RESULTS: KP extract markedly reduced the expression of genes and levels of proinflammatory cytokines, inflammatory mediators, and matrix-degraded enzymes, but neither induced apoptosis nor altered the cell cycle. Its major constituents differently exerted suppressive effects on inflammatory genes. The KP extract downregulated the expression of genes associated with autophagosome and necroptosome formations. The extract also inhibited cell migration, reduced the mRNA expression of cadherin-11, and selectively reduced the phosphorylation of p38 MAPK, STAT1, and STAT3 signaling molecules, but did not interfere with the NF-κB pathway. CONCLUSION: These results suggest that the anti-arthritic potential of KP extract results from anti-inflammation and anti-migration via the suppression of the cytokines-induced p38/STAT1 and STAT3 pathways.