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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. 1. Environmental hyperosmolarity activates NLRP3 inflammasome while suppresses NLRP6 production in primary HCECs.

Fig. 1

(A) mRNA expressions of NLRP3, ASC and NLRP6 by HCECs in hyperosmotic medium (400, 450 and 500mOsM) with isomolar 312mOsM as control, evaluated by RT-qPCR. (B) The protein levels of NLRP3, ASC and NLRP6 in HCECs exposed to iso- and hyper-osmotic medium, evaluated by Western blotting with β-actin as internal control. (C) Caspase-1 activity assay in HCECs with iso- and hyper-osmotic medium. (D) mRNA expression and protein secretion of IL-1β and IL-18 in HCECs exposed to iso- and hyper-osmotic medium, evaluated by RT-qPCR and ELISA. Data shown are representative of three or more independent experiments (mean ± SD). *P < 0.05, **P < 0.01, vs. controls.

HHS Vulnerability Disclosure