https://www.selleckchem.com/EGFR(HER).html
The aforementioned effects of VNS were reversed by cutting the cervical vagus efferent branch and blocking α7nAchR. These findings suggest that VNS inhibits the ARDS inflammatory response by promoting CAIP activity. Next, we used lentivirus knockdown of STAT3 expression to explore the mechanism of VNS through CAIP on lung inflammation in ARDS model rats. VNS activates α7nAchR, increases STAT3 expression, reduces Caspase-1 expression, suppresses inflammation by inhibiting inflammatory pyroptosis and M1 to M2 macrophage transformation, which may
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