Gene interactions and pathways from curated databases and text-mining
Int Immunopharmacol 2009, PMID: 19166983

Hydroxyethyl starch 130/0.4 prevents the early pulmonary inflammatory response and oxidative stress after hemorrhagic shock and resuscitation in rats.

Wang, Pengfei; Li, Yousheng; Li, Jieshou

BACKGROUND

This study was designed to determine the effects of various resuscitation fluids on pulmonary capillary leakage and pulmonary edema after HS and fluid resuscitation (HS/R) and to determine whether an antiinflammatory or antioxidative mechanism was involved.

METHODS

We induced HS by bleeding male Sprague-Dawley rats to a blood pressure of 30 to 40 mm Hg for 60 min. 60 min later, the rats were killed (HS group) or immediately resuscitated with L-isomer lactated Ringer's solution (HS+LR group), shed blood (HS+BL group), or hydroxyethyl starch (HS+HES group) to maintain the blood pressure to the original value during the 60-min resuscitation period. 3 h after resuscitation, pulmonary capillary leakage and wet/dry weight ratio, levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, malondialdehyde (MDA), oxidized and reduced glutathione (GSH and GSSG), myeloperoxidase (MPO) activity, nuclear factor (NF)-kappaB, activator protein (AP)-1 activation, and lung microscopic and ultrastructural histological changes were measured.

RESULTS

HES and BL treatment significantly improved pulmonary capillary leakage, wet/dry weight ratio and lung injuries after HS/R. In addition, both HES and BL could attenuate the increase in TNF-alpha, IL-6, MPO levels and NF-kappaB activation. However, HES but not BL could attenuate the increase in MDA level and GSSH/GSH ratio and AP-1 activation.

CONCLUSIONS

HES might attenuate pulmonary injuries by modulating pulmonary inflammatory response and oxidative stress, whereas BL attenuates pulmonary injuries by modulating pulmonary inflammatory response but not oxidative stress.

Diseases/Pathways annotated by Medline MESH: Disease Models, Animal, Pneumonia, Shock, Hemorrhagic
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Text Mining Data

activator protein (AP)-1 → tumor necrosis factor (TNF)-alpha: " 3 h after resuscitation, pulmonary capillary leakage and wet/dry weight ratio, levels of tumor necrosis factor (TNF)-alpha , interleukin (IL)-6, malondialdehyde ( MDA ), oxidized and reduced glutathione ( GSH and GSSG ), myeloperoxidase (MPO) activity, nuclear factor (NF)-kappaB, activator protein (AP)-1 activation , and lung microscopic and ultrastructural histological changes were measured "

activator protein (AP)-1 → interleukin (IL)-6: " 3 h after resuscitation, pulmonary capillary leakage and wet/dry weight ratio, levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6 , malondialdehyde ( MDA ), oxidized and reduced glutathione ( GSH and GSSG ), myeloperoxidase (MPO) activity, nuclear factor (NF)-kappaB, activator protein (AP)-1 activation , and lung microscopic and ultrastructural histological changes were measured "

TNF-alpha ⊣ HES: " In addition, both HES and BL could attenuate the increase in TNF-alpha , IL-6, MPO levels and NF-kappaB activation "

IL-6 ⊣ HES: " In addition, both HES and BL could attenuate the increase in TNF-alpha, IL-6 , MPO levels and NF-kappaB activation "

MPO ⊣ HES: " In addition, both HES and BL could attenuate the increase in TNF-alpha, IL-6, MPO levels and NF-kappaB activation "

NF-kappaB ⊣ HES: " In addition, both HES and BL could attenuate the increase in TNF-alpha, IL-6, MPO levels and NF-kappaB activation "

AP-1 ⊣ HES: " However, HES but not BL could attenuate the increase in MDA level and GSSH/GSH ratio and AP-1 activation "

Manually curated Databases

No curated data.