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In this study, the central mechanism underlying TAM lipid metabolic reprogramming relies on NP-mediated targeted siCB-2 delivery to TAMs, which silences CB-2 expression, disrupts the 2-AG signaling cascade, and redirects TAM polarization toward the pro-inflammatory M1 phenotype, ultimately restoring anti-tumor immune responses

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Laboratory studies have demonstrated potential neuroprotective effects, including reducing oxidative stress, decreasing inflammation, promoting neuronal survival, and enhancing mitochondrial functionall processes that are impaired in Parkinson's disease