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The mechanism of action of DSePA against RP involved its ability to suppress the radiation-induced sustained inflammatory response by upregulating the pulmonary activity level of GPx and concurrently blocking the NF-kB/IL-17/G-CSF/neutrophil axis (Table 2) (Fig

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EGCG increases spike frequency, reduces resting membrane potential, and reduces afterhyperpolarization amplitude

The commonality is that vascular damage can be mitigated when the factors contributing to glycocalyx degradation are restored to baseline or brought under control