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Considering the rather subtle changes in the gut microbiota and the absence of significant alterations in SCFAs levels, we redirected our focus from microbial mediation towards elucidating the potential mechanism through which HT administration directly mitigates DQ-induced oxidative stress damage in the intestine
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Voltage-gated sodium channels, particularly the Nav1.7, Nav1.8, and Nav1.9 subtypes, play a pivotal role in the generation and propagation of action potentials in pain-sensing neurons [47,48]
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