![]() ![]() Compared with free IL-10, displayed a higher anti-inflammatory effect with fewer mitochondrial disorders ( P < 0.01) and lower expression of NOD-like receptor (NLR)-P3 (NLRP3) ( P < 0.05), resulting in reduced inflammation and pyroptosis in ischemia/reperfusion injury (I/R) mice. could be activated and aggregated, and also released IL-10 at the injury site in the kidney because of high levels of Tumor Necrosis Factor-α (TNF-α). In this system, the PLT drug carrier maintained its original attributes over the study duration, with a good inflammation target effect, confirmed by in vivo imaging. To overcome this challenge, we demonstrate in this study that platelet (PLT) camouflaged IL-10 ( ) can selectively accumulate in injured kidneys for treating kidney inflammation and resulting complications. However, the anti-inflammatory effect of interleukin-10 (IL-10) is largely attenuated because of its insufficient concentration in an injured kidney. Inflammatory factors have emerged as key pathophysiological molecules involved in the progression of acute and chronic kidney disease.
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