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Aim To study the effect of baicalin on the activation of NLRP3 inflammasomes in human fibroblast like synoviocytes of rheumatoid arthritis ( HFLS-RA) and its mechanism. Methods To confirm that baicalin alleviated the activation of NLRP3 inflammasome in HFLS-RA, immunofluorescence was used to observe the expression of NLRP3 before and after baicalin treatment. Western blot was used to detect the protein expression of p-PI3K, p-Akt, NF-κB p65, NL-RP3, ASC and caspase-1 after baicalin treatment for 48 h, and ELISA was employed to detect the contents of IL-1 and IL-18 in the supernatents. In order to explore the mechanism of baicalin alleviating the activation of NLRP3 inflammasome, double luciferin and Westen blot analysis were applied to verify the corresponding relationship between let-7i-3p and PIK3CA. RT-qPCR was utilized to determine the expression of let-7i-3p and PI3K before and after baicalin intervention. let-7i-3p interference was used to verify whether baicalin mitigated the activation of enhanced NLRP3 inflammasomes. Results Baicalin (50, 100 mg · L
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Aim To investigate whether Sal B alleviates hypoxic-induced cardiomyocyte injury by regulating the priming of NLRP3 inflammasomes. Methods The effects of Sal B on growth of H9C2 cells were examined by CCK8 assay,then the appropriate concen tration of Sal B was selected. The expression level of LDH was detected by Microliter assay. The expression levels of cTn/IL-lp were measured by Elisa assay. The protein and mRNA levels of TLR4/Myd88/I-RAK1/NF-kB/NLRP3 were detected by Western blot and qPCR. Results Hypoxia intervention notably reduced the viability of H9C2 cells and increased the expression levels of cTn/IL-IP. Besides,the protein and mRNA expression levels of TLR4/Myd88/IRAK1/NF-kB/NLRP3 were significant uP-regulated after hypoxia intervention. However, the viability of H9C2 cells increased, the secretion levels of LDH/cTn/IL-1 p were reduced,and the protein and mRNA levels of TLR4/Myd88/IRAK1/NF-KB/NLRP3 were significant inhibited after pretreated with Sal B. Conclusion Sal B attenuates cardiomyocyte injury by regulating the priming of NLRP3 inflammasome.I.
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Aim: To investigate whether VGX-1027 could prevent PM2.5-induced mouse lung inflammation and airway hyperresponsiveness. Methods: Fortyeight C57BL/6 mice were randomly divided into control group, VGX-1027(50 mg · kg-1) + PBS group, PM2.5 group, VGX-1027 (12. 5 mg · kg-1) + PM2.5 group, VGX-1027(25 mg · kg-1) + PM2.5 group, and VGX-1027(50 mg · kg-1) + PM2.5 group. Mice were injected intraperitoneally with PBS or corresponding doses of VGX-1027 one hour before intranasal instillation of PBS or PM2.5(7. 8 mg · kg-1) for two consecutive days. 24 hours after last intranasal instillation, airway hyperresponsiveness and bronchoalveolar lavage fluid (BALF) cell numbers were measured. Lung inflammation scores were evaluated by HE staining and the levels of inflammatory cytokines in BALF were detected by ELISA, and the expressed levels of NLRP3 and caspase-1, as well as the phosphorylation levels of NF-kB protein were determined using Western blotting. Results: PM2.5 intranasal instillation induced significant lung inflammation and airway hyperresponsiveness. In the PM2.5 group, VGX-1027 at 12. 5 mg · kg-1 did not inhibit PM2.5-induced airway hyperresponsiveness and lung inflammatory infiltration compared to PM2.5-instilled mice; however, VGX-1027 at 25 and 50 mg · kg-1 inhibited PM2.5-induced airway hyperresponsiveness and lung inflammatory infiltration, decreased the number of inflammatory cells and the levels of inflammatory factors in BALF, and down-regulated NLRP3 and caspase-1 expression, as well as the phosphorylation levels of NF-κB. Conclusion: VGX-1027 could inhibit PM2.5-induced lung inflammation and airway hyperresponsiveness in mice.