Based On NF-κ Exploration Of The B/NLRP3 Signaling Pathway And The Protective Effect Of Buyang Huanwu Deconction On The Inflammation Of HUVECs

Purpose: This project is conducted through TNF-α Injury to human endothelial cells(HUVECs)as a model,using NF-κ Exploring the protective mechanism of Buyang Huanwu Deconction on HUVECs by targeting the B/NLRP3 signaling pathway,providing scientific basis for the further clinical application of Buyang Huanwu Deconction.Method: Using TNF-α A vascular endothelial cell injury model was established at(10ng/ml)for 24 hours.Different concentrations of Buyang Huanwu Deconction(0.5%,1%,2%)were used for intervention.The protective effect of Buyang Huanwu Deconction on cell proliferation was detected using the CCK-8 method,and the apoptosis of each group of cells was detected by flow cytometry.The number of cells was observed with high content,and the expression of ROS in cells was detected by flow cytometry.The expression of NLRP3,ASC,and Caspase-1 m RNA in cells was detected by fluorescence quantitative PCR,Western Blot detection of NF-κB Protein expression ofp65 and NLRP3,Elisa detection of IL-1β in cell culture medium And IL-18 content.Result: 1.Using TNF-α Exploring the Inflammatory Protective Effect of Buyang Huanwu Deconction on Induced HUVECs Injury Model Compared with the normal group,the total number of cells and activity in the model group were significantly reduced,with an increase in apoptotic cells and an increase in ROS content(P<0.05);Compared with the model group,the total number of cells,activity,apoptosis,and ROS content in the low,medium,and high groups of Buyang Huanwu Deconction were significantly increased(P<0.05).2.Using TNF-α Induced HUVECs damage model with NF-κB Exploring the Mechanism of Buyang Huanwu Deconction on HUVECs through the NF-κB/NLRP3 Signal Pathway The low,medium,and high groups of Buyang Huanwu Deconction all downregulated the expression of NLRP3(P<0.05),inhibited the expression of NLRP3 inflammasomes and NLRP3,ASC,and Caspase-1(P<0.05),and showed no significant changes compared to the normal group;Compared with the model group,the low,medium,and high groups of Buyang Huanwu Deconction reduced NF-κB The expression of p65 and NLRP3 proteins(P<0.05);Compared with the model group,the low,medium,and high groups of Buyang Huanwu Deconction can effectively reduce IL-1 β The expression of IL-18 and IL-18(P<0.05).Buyang Huanwu Deconction can effectively downregulate NLRP3 and NF-κB Expression of p65 reduces IL-1β And the release of IL-18 inflammatory factors.Conclusion: 1.Buyang Huanwu Deconction can significantly inhibit TNF-α The induced apoptosis of HUVECs plays a protective role in inflammation.2.Buyang Huanwu Deconction regulates NF-κBp65/NLRP3 signaling pathway improves cell activity and reduces ROS content,downregulates the expression of NLRP3 inflammasomes and NLRP3,ASC,and Caspase-1,and inhibits NF-κB The expression of p65 and NLRP3 proteins reduces IL-1β And the expression of IL-18 plays a protective role.