Fig 1: Changes of hepatic chemokines after iPS infusion in injured mice.(A) iPS-induced changes of cytokines in the liver were evaluated by cytokine array. (B) The hepatic expression of IP-10 and MIG were increased after CCl4 injury. iPS infusion further increase their expressions, but not for iTAC. At 48 h post-injury, the hepatic expression of IP-10 and MIG decreased but IP-10 remained at levels significantly higher than those of the CCl4 group (n = 6, *p<0.05 vs. normal control, # p<0.05 vs. CCl4 group). (C) Hepatic IP-10 at 24 h post-injury was measured in homogenized liver extract by ELISA and western blot. iPS infusion significantly increased hepatic IP-10 in CCl4-injured liver. (n = 4, *p<0.05 vs. normal control, # p<0.05 vs. CCl4 group).
Fig 2: IP-10 is an important factor that mediated the beneficial effects of iPS.(A) Recombinant IP-10 (rIP-10) increased the viability of injured hepatocytes 24 h after CCl4 injury at concentration of 1.0 to 2.5 mM. (B) In injured mice, rIP-10 reduced the degree of liver damage and the effects of rIP-10 were compatible to iPS alone. Combined treatment of rIP-10 and iPS had no additional damage-reducing effects. (C) Anti-IP-10 was used to neutralize the effect of IP-10. Application of anti-IP-10 antibody itself did not exert significant effect but significantly attenuated the reduction of ALT level in the CCl4+iPS group at 24 h after CCl4 injury (n = 6, *p<0.05 vs. CCl4 group, # p<0.05 vs. CCl4+iPS group). (D) In CCl4-injured mice received iPS transfusion, the hepatocyte proliferation at the portal region at 48 h after CCl4 injury was significantly reduced by anti-IP-10 antibody. (E) Survival curve of mice treated with CCl4, CCl4+iPS or rIP-10. All the mice were challenged with CCl4 at time 0, 24 and 48 h (n = 32). At 4 h after initial injury, half of the repetitive injured mice were randomized into two groups to receive iPS (n = 8) or rIP-10 (n = 8) treatment. The survivals of each group were observed until 72 h. Both rIP-10 and IPS treated groups had significant higher survival rates (*p<0.05, n = 6 in each group).
Fig 3: The cellular source and the beneficial effects of IP-10.(A) In vitro cultured iPS secreted IP-10 into culture medium. (B) Mice primary hepatocytes (HC) and none-parenchymal cells (Npc) were isolated from normal and injured mice livers at 24 h post-injury. After iPS infusion, increased expression of IP-10 mRNA were observed mainly in HC from injured liver after iPS treatment (n = 3). (C) Mice none-transformed hepatocytes (AML12) were co-cultured with iPS. iPS increased the viability of the CCl4-injured hepatocytes (n = 3 independent experiment).
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