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. 2023 Jan 31;15(5):1071–1084. doi: 10.1016/j.jcmgh.2023.01.008

Figure 4.

Figure 4

Ninj1-deficient KCs were responsible for decreased expression of proinflammatory cytokines and CXCL-1 both ex vivo and in vitro. WT→WT and KO→WT mice were subjected to 90 minutes of warm ischemia or a sham procedure, and liver tissues were collected at 24 hours after reperfusion. KCs were isolated from livers of each group and were cultured in vitro for 3 hours. The cells and culture supernatant were collected. (A) Quantitative RT-PCR analysis of KC inflammatory cytokine and chemokine gene induction (IL6, IL1β, TNF-α, CXCL-1, and CXCL-2). (B) Enzyme-linked immunosorbent assay of inflammatory cytokine and chemokine levels in cells supernatant. KCs isolated from WT and Ninj1 KO mice were stimulated with LPS for 6 hours. The cells and culture supernatant were collected. (C) Quantitative RT-PCR analysis of KC inflammatory cytokine and chemokine gene induction (IL6, IL1β, TNF-α, CXCL-1, and CXCL-2). (D) Enzyme-linked immunosorbent assay of inflammatory cytokine and chemokine levels in cell supernatant. All results are representative of at least 2 independent experiments. ∗P < .05. All data are presented as the means ± SD. GAPDH, glyceraldehyde-3-phosphate dehydrogenase; PBS, phosphate-buffered saline.