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. 2024 Sep 12;18(6):101402. doi: 10.1016/j.jcmgh.2024.101402

Figure 6.

Figure 6

MT2 inhibition abolishes XBP1M-KO-related anti-inflammatory features in vivo and in vitro. The IRI model mice were subjected to 90-minute ischemia, followed by 6-hour reperfusion. (A) XBP1M-KO mice were injected with siRNA-MT2 by caudal vein before establishing hepatic IRI model. (B) Western blotting analysis for the expressions of MT2 in nonparenchymal cells (NPC) after siRNA-MT2/siRNA-NC was injected into mice tail vein. (C) Serum ALT and AST levels were measured. (D) Detection of TNF-α, IL1β, IL6, iNOS, and IL10 in the ischemic liver of mice by qRT-PCR. (E) HE DCFH, TUNEL, F4/80, CD11b, and Ly6G staining, and (F, H) their quantitations. (G) Expressions of Bcl-2, Bcl-xl, C-caspase 3, P-NF-κBp65, and NF-κBp65 in IR liver tissues based on Western blotting analysis. (I) Detection of TNF-α, IL1β, IL6, iNOS, and IL10 in H/R cocultured XBP1M-KO BMMs through qRT-PCR. (J) Western blotting analysis for the expressions of MT2 in BMMs after transfected with siRNA-MT2/siRNA-NC. (K) Migratory abilities of XBP1M-KO BMMs cocultured for 24 hours based on the Transwell assay. (L) Expressions of NLRP3, MT2, IKBα, P-NF-κBp65, and NF-κBp65 in H/R cocultured XBP1M-KO BMMs using Western blotting assay. n = 6, ∗P < .05 by Student t test.