A single dose of carbon monoxide intraperitoneal administration protects rat intestine from injury induced by lipopolysaccharide

Abstract

Treatment with inhaled carbon monoxide (CO) has been shown to ameliorate intestinal injury induced by lipopolysaccharide (LPS) or ischemia-reperfusion in experimental animals. We hypothesized that CO intraperitoneal administration (i.p) might provide similar protection against inhaled gas. In the present study, 1 h after intravenously receiving 5 mg/kg LPS, rats were exposed to either room air or 2 ml/kg of 250 ppm CO i.p for 1, 3, and 6 h. Intestinal tissues were collected to determine the levels of platelet activator factor (PAF), intercellular adhesion molecule-1 (ICAM-1), interleukin-10 (IL-10), maleic dialdehyde (MDA), cell apoptotic rate and the phosphorylated p38 mitogen activated protein kinase (MAPK), as well as myeloperoxidase (MPO) and superoxide dismutase (SOD) activity. After CO i.p, the increase of PAF, ICAM-1, MDA, MPO, and cell apoptosis rate induced by LPS was markedly reduced (P < 0.05 or 0.01), while the decrease of IL-10 and SOD was significantly increased (P < 0.05). Western blotting showed that the effects of CO i.p were mediated by p38 MAPK pathway. Thus, the results of our study show that CO i.p exerts potent protection against LPS induced injury to the intestine via anti-oxidant, anti-inflammation and anti-apoptosis, which may involve the p38 MAPK pathway.

Fig. 1

Effects of CO i.p on intestinal MDA

Fig. 2

Effects of CO i.p on intestinal MPO activity

Fig. 3

Effects of CO i.p on intestinal SOD activity

Fig. 4

Effects of CO i.p on intestinal PAF

Fig. 5

Effects of CO i.p on intestinal ICAM-1

Fig. 6

Effects of CO i.p on intestinal IL-10

Fig. 7

Effects of CO i.p on intestinal cells apoptosis

Fig. 8

Effects of CO i.p on the expression of the phosphorylated p38 MAPK

Fig. 9

CO i.p ameliorates LPS-induced intestine injury