The role of different subtypes of G protein in the secretory function of macrophages stimulated by activated complement following severe burn injury / 中华烧伤杂志

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the influence of activated complement on the secretory function of peritoneal macrophage (PMphi) in the production of nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha), especially in the role of different G-protein subtypes in this process after burns.</p><p><b>METHODS</b>The mice inflicted by 18% TBSA full-thickness scald was established and employed as the model. And the mice were divided into A (the complements were preserved and activated) and B (with intraperitoneal injection of CVF to deplete complement before scald) groups. The plasma of the mice in the two groups was collected at 6 postburn hour (PBH) and cultured with PMphi from normal mice. The PMphi were pretreated with pertussis toxin (PT) and with cholera toxin (CT). The NO and TNF-alpha levels in the supernatant of normal PMphi culture with different pretreatment were measured by Greiss assay.</p><p><b>RESULTS</b>The NO and TNF-alpha contents in group A [(80 +/- 12) micromol/L, (46 +/- 6)%] were obviously higher than those in group B [(34 +/- 5) micromol/L, (26 +/- 5)%, P < 0.01]. The NO content produced by PMphi (45 +/- 10 micromol/L) in A group decreased (P < 0.01), while the TNF-alpha activity (58 +/- 10)% increased by PT pretreatment (P < 0.05). On the contrary, the NO content produced by PMphi (105 +/- 18 micromol/L) in group A increased (P < 0.01), while the TNF-alpha activity (27 +/- 6)% decreased by CT pretreatment (P < 0.01).</p><p><b>CONCLUSION</b>These results indicates that the secretory function of normal PMphi can be enhanced by complement activation after thermal injury, which might partly be due to the effect of activated complement components through complement receptor coupled G-protein. In the secretory function of complement stimulated Mphi, Gi protein has a major role in the production of NO, Gs protein is mainly involved in the secretion of TNF-alpha.</p>