Research Paper Volume 14, Issue 17 pp 6905—6916

NOX4 promotes Kupffer cell inflammatory response via ROS-NLRP3 to aggravate liver inflammatory injury in acute liver injury

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Figure 2. NOX4 promotes inflammatory factor expression and NLRP3 inflammasome activation. (A) Results of cell viability assay (n = 3). NOX4 promoted the down-regulation of cell viability. The cell viability in L/N-NOX4 group significantly decreased compared with L/N-Con group. *P < 0.05, compared with Con group; #P < 0.05, compared with NOX4 group; P < 0.05, compared with L/N-Con group. (BD) Expression of inflammatory factors (n = 3). LPS and Nigericin promoted the expression and release of inflammatory factors, and the levels of IL-6, TNF-α and IL-1β were significantly higher than those in Con and NOX4 groups. While the expression of inflammatory factors in L/N-NOX4 group further increased, higher than that in L/N-Con group. *P < 0.05, compared with Con group; #P < 0.05, compared with NOX4 group; P < 0.05, compared with L/N-Con group. (E, F) Detection of protein expression (n = 3). LPS and Nigericin promoted NLRP3 activation, and the levels of NLRP3, ASC and Caspase-1 significantly increased. NOX4 overexpression further promoted NLRP3 activation, and the levels of NLRP3, ASC and Caspase-1 in L/N-NOX4 group were higher than those in L/N-Con group. *P < 0.05, compared with Con group; #P < 0.05, compared with NOX4 group; P < 0.05, compared with L/N-Con group.