Fig 1: Suppression of CMPK2 alleviates I/R-induced deterioration of hepatic injury. (A) Protein detection of CMPK2 in liver tissue. Secretion of (B) IL-18 and (C) IL-1β was measured by ELISA. Hepatocellular function of experimental mice was evaluated by detecting the release of (D) AST and (E) ALT. (F and G) Histological changes of the liver in the sham, I/R, I/R + scramble siRNA and I/R + CMPK2 siRNA groups. Original magnification, x200. **P<0.01, ***P<0.001 vs. sham group; #P<0.05, ##P<0.01 vs. I/R group. CMPK2, cytidine monophosphate kinase 2; NLRP3, NLR family pyrin domain containing 3; I/R, ischemia/reperfusion; siRNA, small interfering RNA; ALT, alanine aminotransferase; AST, aspartate aminotransferase.
Fig 2: Knockdown of CMPK2 decreased the NLRP3-associated inflammation factor. (A) Protein detection of CMPK2 after H/R treatment in scramble siRNA or CMPK2 siRNA-transfected RAW 264.7 cells. (B) Western blotting and subsequent quantification of (C) CMPK2, (D) NLRP3, (E) AIM2, (F) pro-IL-1β, (G) cleaved-caspase-1 (H) IL-1β and (I) IL-18 protein levels. (J) IL-18 and IL-1β levels in the supernatant were detected by ELISA. **P<0.01, ***P<0.001 vs. control group, #P<0.05, &&P<0.01 vs. H/R group. CMPK2, cytidine monophosphate kinase 2; NLRP3, NLR family pyrin domain containing 3; H/R, hypoxia/reoxygenation; siRNA, small interfering RNA; AIM2, absent in melanoma 2.
Fig 3: Knockdown of CMPK2 decreases IL-18 and IL-1β by inhibiting the NLRP3 inflammasome, and not AIM2. Protein detection of (A) NLRP3 or (B) AIM2 following H/R treatment in scramble siRNA or specific siRNA-transfected RAW 264.7 cells. (C) Protein detection and respective quantification of (D) cleaved-caspase-1, (E) IL-18 and (F) IL-1β in the H/R + CMPK2 siRNA, H/R + CMPK2 siRNA + NLRP3 siRNA, and H/R + CMPK2 siRNA + AIM2 siRNA groups. ##P<0.01 vs. H/R +CMPK2 siRNA group. CMPK2, cytidine monophosphate kinase 2; NLRP3, NLR family pyrin domain containing 3; H/R, hypoxia/reoxygenation; AIM2, absent in melanoma 2; siRNA, small interfering RNA.
Fig 4: mRNA expression levels of CMPK2, NLRP3 and inflammatory factors in H/R model of RAW 264.7 cells. (A) The mRNA levels of CMPK2 were measured at different time points after reoxygenation. The mRNA expression levels of (B) NLRP3, (C) TNF-α, (D) IL-1β and (E) IL-18 were detected following H/R treatment. *P<0.05, **P<0.01 vs. control groups. CMPK2, cytidine monophosphate kinase 2; NLRP3, NLR family pyrin domain containing 3; H/R, hypoxia/reoxygenation.
Fig 5: CMPK2 Upregulation in LPS-Stimulated BV2 Cells. (A) Analysis of CMPK2 mRNA expression under different concentrations of LPS treatment. (B) Analysis of CMPK2 mRNA expression at different time points following LPS treatment. The presented data represent the mean ± standard deviation (SD) derived from three independent experiments. Statistical significance of the fold change was determined, with ****P < 0.0001 denoting the significance levels.
Supplier Page from Abcam for Anti-CMPK2 antibody