RESUMEN
Gouty arthritis (GA), a metabolic and immunologic disease, primarily affects joints. Dysbiosis of intestinal flora is an important cause of GA. The metabolic disorders of intestinal flora leading to GA and immune disorders might play an important role in patients with hyperuricemia and established GA. However, the exact mechanisms, through which the dysbiosis of intestinal flora causes the development of GA, are not fully understood yet. Moreover, several therapies commonly used to treat GA might alter the intestinal flora, suggesting that modulation of the intestinal flora might help prevent or treat GA. Therefore, a better understanding of the changes in the intestinal flora of GA patients might facilitate the discovery of new diagnostic and therapeutic approaches. The current review article discusses the effects of intestinal flora dysbiosis on the pathogenesis of GA and the cross-regulatory effects between gut flora and drugs for treating GA. This article also highlights the modulatory effects of gut flora by traditional Chinese medicine (TCM) to lower uric acid levels and relieve joint pain as well as provides a summary and outlook, which might help guide future research efforts.
Asunto(s)
Artritis Gotosa , Disbiosis , Microbioma Gastrointestinal , Ácido Úrico , Artritis Gotosa/microbiología , Artritis Gotosa/tratamiento farmacológico , Humanos , Disbiosis/microbiología , Ácido Úrico/metabolismo , Medicina Tradicional China , Animales , HiperuricemiaRESUMEN
In this article, a nanosurface molecularly imprinted polymer (MQD@MIP) resonance Rayleigh scattering (RRS) spectral probe for SCN- was prepared by sol-gel method, using Mxene quantum dot as a matrix, thiocyanate (SCN-) as a template ion, (3-aminopropyl) triethoxysilane (APTES) as a functional monomer, tetraethoxysilane (TEOS) as the cross-linker, and ammonia as the initiator. The probe produced an RRS peak at 370 nm and exhibits a strong RRS energy transfer (RRS-ET) effect when the MQD@MIP probe identifies SCN-. As the concentration of SCN- increased, the RRS-ET was enhanced, and the signal value of the system decreased linearly at 370 nm, with a determination range of 0.87-5.22 µg/L, and a detection limit of 0.37 µg/L SCN-. This detection method has the characteristics of simplicity, sensitivity, and specific recognition. The RRS method was used to determine SCN- in the sample, with relative standard deviation of 1.95-10.98% and recovery of 89.0-102.8%.
RESUMEN
Therapeutic oligonucleotides, such as antisense DNA, show promise in treating previously untreatable diseases. However, their applications are still hindered by the poor membrane permeability of naked oligonucleotides. Therefore, it is necessary to develop efficient methods for intracellular oligonucleotide delivery. Previously, our group successfully developed disulfide-based Membrane Permeable Oligonucleotides (MPON), which achieved enhanced cellular uptake and gene silencing effects through an endocytosis-free uptake mechanism. Herein, we report a new molecular design for the next generation of MPON, called trimer MPON. The trimer MPON consists of a tri-branched backbone, three α-lipoic acid units, and a spacer linker between the oligonucleotides and tri-branched cyclic disulfide unit. We describe the design, synthesis, and functional evaluation of the trimer MPON, offering new insights into the molecular design for efficient oligonucleotide delivery.
RESUMEN
Post-stroke depression (PSD) is a psychological disease that can occur following a stroke and is associated with serious consequences. Research on the pathogenesis and treatment of PSD is still in the infancy stage. Patients with PSD often exhibit gastrointestinal symptoms; therefore the role of gut microbiota in the pathophysiology and potential treatment effects of PSD has become a hot topic of research. In this review, describe the research on the pathogenesis and therapy of PSD. We also describe how the gut microbiota influences neurotransmitters, the endocrine system, energy metabolism, and the immune system. It was proposed that the gut microbiota is involved in the pathogenesis and treatment of PSD through the regulation of neurotransmitter levels, vagal signaling, hypothalamic-pituitary-adrenal axis activation and inhibition, hormone secretion and release, in addition to immunity and inflammation.