Abstract
The relationship between intensity of inflammatory stimulation and production of α 2-macroglobulin (α2M) and α 1-acid glycoprotein (AAG) in rats was investigated. Sprague-Dawley rats were injected with turpentine oil at doses of 0.05, 0.2 or 0.4 mL/rat. Serum levels of α2M, interleukin (IL)-6 and cytokine-induced neutrophil chemoattractant-1 (CINC-1) were measured by enzyme-linked immunosorbent assay, and AAG was measured by single radial immunodiffusion. Peak serum levels of α2M and AAG in rats injected at 0.05 mL/rat were significantly lower than those at 0.2 or 0.4 mL/rat. However, no significant differences were observed for peak serum levels of these acute-phase proteins between 0.2 and 0.4 mL/rat. Furthermore, peak serum levels of IL-6 and CINC-1 in rats injected at 0.05 mL/rat were significantly lower than those at 0.2 or 0.4 mL/rat. Thus, the production of these acute-phase proteins has upper limits, even under increased strength of inflammatory stimulation in rats injected with turpentine oil.
Highlights
C-reactive protein is a typical acute-phase protein in humans and dogs,[4,5,6,7] while a2-macroglobulin (a2M) is a typical acute-phase protein in rats.[8,9,10] a2M levels increase in rats subjected to acute inflammation by inoculation with microorganisms, injection of turpentine oil or after surgical treatment.[9] a1-acid glycoprotein (AAG) contributes to protein binding with anionic drug substances, and increases following inflammatory stimulation.[11,12]
Serum levels of a2M and AAG in rats injected with 0.05 mL/rat were significantly lower than those injected with 0.2 and 0.4 mL/rat; no significant differences were observed between the 0.2 and 0.4 mL/rat injection groups. These results suggest that production of a2M and AAG increases in proportion with turpentine oil dose
IL-6 is known to regulate the synthesis of acute-phase proteins,[17,18,19,20,21,22] while IL-8 regulates the production of acutephase proteins in humans.[23,24]
Summary
Acute-phase protein levels increase during acute inflammation, e.g. bacterial infection, trauma and surgical treatment.[1,2,3] C-reactive protein is a typical acute-phase protein in humans and dogs,[4,5,6,7] while a2-macroglobulin (a2M) is a typical acute-phase protein in rats.[8,9,10] a2M levels increase in rats subjected to acute inflammation by inoculation with microorganisms, injection of turpentine oil or after surgical treatment.[9] a1-acid glycoprotein (AAG) contributes to protein binding with anionic drug substances, and increases following inflammatory stimulation.[11,12]. Peak levels of AAG differ after injection of turpentine oil, inoculation with microorganisms and gastric bleeding by injection of indomethacin.[12] Peak levels of these acute-phase proteins are presumed to differ with the magnitude of inflammatory stimulation in rats. The changes in serum levels of a2M and AAG in rats subjected to various dosages of turpentine oil to induce acute inflammation were investigated in an effort to clarify whether the production of acute-phase proteins varies with the magnitude of inflammatory stimulation
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