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. 2021 May 13;12:652782. doi: 10.3389/fimmu.2021.652782

Figure 4.

Figure 4

PRX3 regulates NLRP3-mediated pyroptosis in APAP-induced hepatotoxicity in vitro. Primary KCs and hepatocytes were transfected with NLRP3-specific siRNA and then exposed to APAP (10 mM). (A) Kupffer cellular supernatant levels of LDH were assessed, n=6. (B) NLRP3, GSDMD-N, caspase-1 p20, IL-1β, and IL-18 protein levels in primary KCs, n=3. (C) Hepatocellular supernatant levels of LDH were assessed, n=6. (D) NLRP3, GSDMD-N, caspase-1 p20, IL-1β, and IL-18 protein levels in primary hepatocytes, respectively, n=3. (E) Primary hepatocytes were transfected with pcDNA-PRX3 and then exposed to APAP (10 mM). PRX3, GSDMD-N, caspase-1 p20, IL-1β, and IL-18 protein levels in primary hepatocytes were determined, n=3. (F) Hepatocellular supernatant levels of LDH were assessed, n=6. (G) NLRP3 protein levels in primary hepatocytes, n=3. (H) Double immunofluorescence staining for PRX3 and NLRP3 in primary hepatocytes, 50 μm. (I) Hepatocellular supernatant levels of LDH were assessed, n=6. (J) Primary hepatocytes were transfected with si-PRX3 and then exposed to APAP (10 mM). PRX3, GSDMD-N, caspase-1 p20, IL-1β and IL-18 protein levels in primary hepatocytes were determined, n=3. (K) NLRP3 protein levels in primary hepatocytes, n=3. **P<0.01, *P<0.05.