Preventive effects and mechanism of heme oxygenase-1 activation on acute respiratory distress syndrome in rats.
- Author:
Jing CHEN
1
;
Jin-yuan ZHAO
;
Guang-zeng WANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Blotting, Western; Bronchoalveolar Lavage Fluid; chemistry; Enzyme-Linked Immunosorbent Assay; Heme Oxygenase-1; biosynthesis; genetics; Hemoglobins; pharmacology; Interleukin-8; metabolism; Male; Oleic Acid; RNA, Messenger; genetics; Rats; Rats, Sprague-Dawley; Respiratory Distress Syndrome, Adult; metabolism; prevention & control; Reverse Transcriptase Polymerase Chain Reaction; Tumor Necrosis Factor-alpha; metabolism
- From: Chinese Journal of Industrial Hygiene and Occupational Diseases 2005;23(3):199-202
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the possible mechanism of heme oxygenase-1 (HO-1) induction for its protective effects on acute respiratory distress syndrome (ARDS).
METHODSThe production of HO-1 was induced by hemoglobin (Hb) injection into oleic acid (OA) induced ARDS rats. Western blot and RT-PCR techniques were used to observe the induction of HO-1 in vivo. Both the levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin-8 (IL-8) in serum and bronchoalveolar lavage fluid (BALF) were measured by enzyme linked immunosorbent assay (ELISA). Combined with blood gas analysis and other indexes, the effect of HO-1 on ARDS could be clearly manifested.
RESULTSThe expression of HO-1 mRNA was increased significantly 16 h after Hb injection, and the protein expression of HO-1 was also obviously increased 24 h later (P < 0.01). The levels of TNF-alpha and IL-8 in both serum and BALF were significantly lower in Hb + OA group than in OA group (P < 0.01). Arterial blood PaO(2), oxygen saturation, and oxygenated index in Hb + OA group [(56.28 +/- 6.71) mm Hg, (79.53 +/- 5.82)%, and (258.81 +/- 29.37) mm Hg respectively] were higher than in OA group [(35.08 +/- 4.59) mm Hg, (55.80 +/- 12.76)%, and (167.86 +/- 21.94) mm Hg]. Lung wet and dry weight, and pathological changes were also improved.
CONCLUSIONThe production of HO-1 was successfully induced by hemoglobin in vivo. Protective effects of HO-1 on ARDS might be related to the decreasing in inflammatory factors, such as TNF-alpha and IL-8.