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. 2020 May 26;11(5):394. doi: 10.1038/s41419-020-2609-7

Fig. 3. Upregulated cAMP suppressed acute gouty arthritis in vivo.

Fig. 3

As a potent adenylate cyclase (AC) activator, Forskolin is used to increase the intracellular level of the second messenger cAMP. Intra-articular administration of Forskolin was given to WT rats prior to MSU induction. a The intracellular cAMP level in synovial tissue increased significantly after Forskolin treatment (n = 6). b cAMP elevation induced by Forskolin prevented the joint swelling. Representative photographs to show the swelling of joints are presented. c Forskolin-induced cAMP elevation alleviated the injected ankle joint circumference under MSU challenge (n = 6). d Forskolin treatment efficiently inhibited inflammatory cell infiltration when compared MSU group in histopathologic test. e The macrophages derived from synovium of Forskolin-treated rats exhibited a lower positivity of active Caspase-1 and PI double staining in pyroptosis assay by flow cytometry (n = 4). f Forskolin treatment inhibited the colocalization intensity of NLRP3 and ASC in MSU-stimulated WT animals in immunofluorescence staining. NLRP3 protein was marked with Alexa Fluor 488 (Green). ASC protein was marked with Alexa Fluor 647 (Red). DAPI (Blue) was used to mark the nucleus. g Western blotting showed Forskolin treatment inhibited MSU-induced NLRP3 inflammasome activation in WT rats. The relative optical density was exhibited in the supplementary materials (n = 4). The data were presented as means ± SDs. Compared with WT + vehicle group: #P < 0.05, ##P < 0.01, ###P < 0.001. Compared with WT + MSU group: *P < 0.05, **P < 0.01, ***P < 0.001.