Abstract
To study the expression and relationship of cyclooxygenase-2(COX-2) and peroxisome proliferators activated receptor-γ (PPARγ) in peripheral blood monouclear cells (PBMCs) of multiple organ dysfunction syndrome patients. In the emergency department and intensive care unit (ICU) of our hospital, 60 MODS patients were divided into three groups with 20 cases in each group. They were MODS1 group (APACHE II score 0-10 points), MODS 2 groups (APACHE II score 11-20 points), MODS 3 groups (APACHE II score> 20 points) and control groups of 20 healthy subjects. Venous blood were sampled 1d, 3d, 6d after diagnosis of MODS, reverse transcriptase -polymerase chain reaction (RT-PCR) were used to detect the expression of PPARγ, COX-2 in PBMCs. The expression of PPARγ, COX-2 in the same period were compared between the MODS groups and the healthy control group. The study fond that the expression of COX-2 and PPARγ were low in vehicle control group. In MODS1 group the expression of PPARγ and COX-2 was higher than in vehicle control group; during the treatment period, PPARγ was significantly increased (P <0.05), but the expression of COX-2 was significantly lower (P <0.05). PPARγ expression in MODS 2 group and MODS 3group was lower than that in vehicle control group, and its expression was progressively decreased during the treatment (P <0.05);in contrast, Expression of COX-2 in MODS2 and MODS3 group was higher than that in vehicle control group, and its level was progressively increased during the treatment (P <0.05). The study revealed a significant negative correlation between COX-2 and PPARγ in MODS1 group, MODS2 group and MODS3 group. (MODS1 group r=-0.761, P<0.01; MODS2 group: r=-0.782, P<0.01; MODS3 group: r=-0.791, P<0.01). There was no significant correlation in vehicle control group (r = -0.185, P >0.05). Thus, PPARγ may protect the MODS patients by repressing the expression of cox-2 therefore it can be used as an important indicator and potential target to determine the condition and treatment of MODS.
Highlights
Multi-organ dysfunction syndrome (MODS) is the greatest challenge to critically ill medicine, with high morbidity and mortality and no satisfactory treatment
Arachidonic acid metabolites generated by cox-2 - delta - 15 - to oxygen (12, 14) prostaglandin J2 (15 d - PGJ2), is the most important natural endogenous ligand of PPAR gamma, combined with PPAR gamma, by inhibiting the activity of cox-2, inhibiting the expression of inflammatory factor, the synthesis of cox-2 regulation; In addition, the 15d-pgj2 can be combined with the PPAR gamma receptor in the nucleus to reduce cox-2 activity through the PPAR gamma-cox-2 negative feedback pathway
The expression of PPAR gamma mRNA in normal group peripheral blood monouclear cells (PBMCs) was less, and compared with normal group, the expression of PPAR gamma mRNA in MODS1 group was higher and higher in time, reaching the peak value of the 6th day (P < 0.05)
Summary
Multi-organ dysfunction syndrome (MODS) is the greatest challenge to critically ill medicine, with high morbidity and mortality and no satisfactory treatment. In the in vivo and in vitro experiments found that PPAR gamma and its ligands in the cell molecular level control inflammation and immune response, the activation of PPAR gamma by blocking cox-2 to implement is immune to all kinds of factors which can adjust the immune function. Cox-2 is induced enzyme, not express or trace expression in normal tissue, but in the body "severe trauma, infection, shock" stimulating factors, the expression of cox-2 rapid increase [2], inducing the synthesis of a variety of PGs, causes the body's inflammatory response to be amplified and continuous development, cox-2 is activated at the same time after can inhibit the release of TNF alpha and other cytokines, have anti-inflammatory effect. Arachidonic acid metabolites generated by cox-2 - delta - 15 - to oxygen (12, 14) prostaglandin J2 (15 d - PGJ2), is the most important natural endogenous ligand of PPAR gamma, combined with PPAR gamma, by inhibiting the activity of cox-2, inhibiting the expression of inflammatory factor, the synthesis of cox-2 regulation; In addition, the 15d-pgj can be combined with the PPAR gamma receptor in the nucleus to reduce cox-2 activity through the PPAR gamma-cox-2 negative feedback pathway
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