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"Then we detected the activation of NLRP3 inflammsome pathway in rats during cerebral I/R injury, and found that the diazoxide could inhibit the activation of NLRP3 inflammasome, which indicated that mitochondrial dysfunction played a great role in activating NLRP3 inflammasome in cerebral I/R injury."

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"In addition, diazoxide could also suppress the upregulation of NLRP3, ASC, and cleaved caspase 1induced by OGD/R in primary microglia and BV2 cells (all p < 0.01)."

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"We further demonstrated that the mitochondrial protector diazoxide was able to reduce NLRP3 upregulation in a post-operative treatment paradigm."

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"Mitochondrial dysfunction plays an important role in the activation of NLRP3 after ischemia/reperfusion in rats, while diazoxide, a mitochondrial protectant, can inhibit the activation of NLRP3 in bra[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"