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. Author manuscript; available in PMC: 2018 Jun 1.
Published in final edited form as: J Autoimmun. 2017 Feb 24;80:65–76. doi: 10.1016/j.jaut.2017.02.006

Fig. 2. Inhibition of NLRP3 or caspase-1 activity reverses the reciprocal regulation of NLRP3 and NLRP6, and blocked caspase-1-dependent secretion of IL-1β and IL-18.

Fig. 2

(A and B) mRNA and protein levels of NLRP3, ASC and NLRP6 in HCECs at 450mOsM without or with addition of glybenclamide (30μM), a NLRP3 inhibitor (P3-Inh), compared with isomolar controls at 312 mOsM. (C) Caspase-1 activity assay in HCECs at 450mOsM without or with P3-Inh. (D and E) Cleavage and secretion of proIL-1β and proIL-18 in HCECs at 450mOsM without or with P3-Inh. (F and G) Protein and mRNA levels of NLRP3 and NLRP6 in HCECs at 450mOsM without or with 20μM of caspase-1 inhibitor z-YVAD fmk (C1-Inh). (H and I) Cleavage and secretion of proIL-1β and proIL-18 in HCECs at 450mOsM without or with C1-Inh. Data shown are representative of three or more independent experiments (mean ± SD). *P < 0.05, **P < 0.01, vs. controls.

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