Microneedles enhance gout treatmentTransdermal delivery of colchicine using dissolvable microneedle arrays for the treatment of acute gout in a rat model.
We explored a new approach to treating acute gout using dissolvable microneedles filled with colchicine, a well-known medication for this condition. The microneedles were created with hyaluronic acid, an ingredient often used in skincare, and designed for transdermal delivery—meaning they can deliver medication through the skin without needing needles like those found in injections.
During our study, we evaluated the mechanical properties of these microneedles, ensuring they could effectively penetrate the skin and release the medication. Importantly, our findings showed that using these microneedles allowed for a significant increase in the amount of colchicine that entered the bloodstream compared to traditional gel applications. We also noted no skin irritation after application, indicating that this method is not only effective but also gentle on the skin.
Furthermore, we found that this method significantly reduced swelling and pain in rats with acute gout. By minimizing the gastrointestinal side effects commonly associated with oral colchicine, we hope this innovative delivery system can enhance treatment effectiveness and improve patient adherence to medication. Overall, our study suggests that using hyaluronic acid in microneedles could be a promising way to deliver colchicine for better gout management.
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Potential BHA treatment for gout-Butyrylated Hyaluronic Acid Achieves Anti-Inflammatory Effects In Vitro and in Adjuvant-Induced Immune Activation in Rats.
We aimed to explore how butyrylated hyaluronic acid (BHA) can help with the inflammation associated with gout. In our investigation, we looked at BHA's anti-inflammatory and antioxidative powers using both laboratory tests with LPS-induced cells and a live rat model that simulates gout.
Our results were promising. We saw that BHA significantly reduced the production of key inflammatory molecules, like TNFα, IL-1β, and IL-6, which are all often elevated during gout attacks. Additionally, it reduced the production of harmful reactive oxygen species, which can contribute to inflammation. In the rat model, BHA not only alleviated swelling in the joints and paws, but also decreased the infiltration of inflammatory cells in the affected tissues.
Furthermore, we noted that BHA appeared to work by influencing several important cell signaling pathways that are known to drive inflammation. Specifically, it down-regulated pathways associated with inflammation, providing a further line of evidence for its potential use in treating conditions like gout.
Overall, our study highlights the potential of BHA as a novel treatment option for managing gout-related inflammation, making it a candidate for future pharmacological development.
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BHA shows promise for gout relief-Butyrylated hyaluronic acid ameliorates gout and hyperuricemia in animal models.
We explored the benefits of butyrylated hyaluronic acid (BHA) in treating gout by examining its effects in specific animal models. Using Wistar rats, we evaluated how BHA can influence inflammation linked with gouty arthritis, specifically by measuring joint swelling and inflammatory markers after injecting monosodium urate crystals.
Our findings showed that a higher dose of BHA (50 μg) effectively reduced joint swelling and lowered levels of key inflammatory cytokines, indicating a strong anti-inflammatory effect. In another part of our study, we assessed BHA’s impact on hyperuricemia in Balb/C mice, where lower doses (10 μg) were sufficient to exhibit antioxidative properties and significantly decrease uric acid levels.
This first-of-its-kind study suggests that BHA could be a promising approach to alleviate symptoms associated with gouty arthritis and manage hyperuricemia. Overall, our research highlights BHA's potential therapeutic role in addressing these painful conditions.
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Hyaluronic acid eases gout painJoint nociceptor nerve activity and pain in an animal model of acute gout and its modulation by intra-articular hyaluronan.
We explored how hyaluronic acid (HA) can be beneficial in managing the pain and inflammation caused by gout. In our study, we injected rats with monosodium urate (MSU) crystals, mimicking the painful arthritis associated with gout. We observed that this injection resulted in significant joint swelling, increased pain sensitivity, and heightened nerve activity indicative of pain.
The exciting part of our findings was that after administering HA into the joint, there was a notable reduction in these painful symptoms. The HA appeared to not only alleviate the behavioral signs of pain but also diminish the heightened nerve activity linked with the gout flare-up.
Our investigation suggests that the pain and nerve activation induced by MSU crystals are not solely due to mechanical irritation but rather stem from inflammatory responses triggered by these crystals. HA seems to ease the discomfort, possibly by filtering out some of the mechanical stress placed on the sensitive nerve endings in the joint and by interacting with the pain receptors directly.
Overall, the results indicate that hyaluronic acid could be a promising treatment option for individuals suffering from gout, helping to manage the pain and improve their quality of life.
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Chondroitin sulfate shows promise for goutMonosodium urate crystal induced macrophage inflammation is attenuated by chondroitin sulphate: pre-clinical model for gout prophylaxis?
We explored the potential benefits of chondroitin sulfate (CS) in managing gout, particularly its effects on inflammation triggered by monosodium urate (MSU) crystals. To understand this, we conducted an in vitro study using THP-1 monocytes, which were turned into macrophages. After treating these cells with CS at various doses, we stimulated them with MSU crystals.
Our findings revealed that MSU crystals significantly increased the production of pro-inflammatory cytokines like IL-1β, IL-8, and TNFα in macrophages. Interestingly, when CS was introduced, it reduced the levels of IL-1β and TNFα in a dose-dependent manner, indicating its potential anti-inflammatory properties. Although CS also suggested a decrease in IL-8, it wasn't statistically significant.
These results suggest that chondroitin sulfate could play a beneficial role in mitigating inflammation associated with gout. However, while our study presents promising findings, it still requires further investigation, especially in clinical settings to fully ascertain its effectiveness for gout sufferers.
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