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Hypertension, conversely, upregulates endothelial FAO, reducing nitric oxide bioavailability and capillary perfusion, explaining why hypertensives gain 50% less reperfusion benefit post-thrombectomy [122, 130, 131]

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Studies (85, 86) have shown that the anti-inflammatory mechanism of tetrandrine in the treatment of RA may be related to its efficacy in inhibiting the LPS-induced phosphorylation of IB and NF-B p65 in RAW 264.7 macrophages and ATDC5 chondrocytes and reducing the expression of COX in peripheral blood mononuclear cell of CFA rats

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