- Time Course of Inducible NOS Expression of Lung Tissue during Sepsis in a Rat Model
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Joong Hee Kim, Seong Chun Kim, Woon Yong Kwon, Gil Joon Suh, Yeo Kyu Youn
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J Korean Soc Traumatol. 2008;21(2):120-127.
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 Abstract
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- PURPOSE
Many studies on the time course of inducible nitric oxide synthase (iNOS) gene expression have been performed in the LPS (Lipopolysaccharide)-induced endotoxemic model, but there have been few experimental approaches to continuous peritonitis-induced sepsis model. We conducted this study to establish basic data for future sepsis-related research by investigating the time course of iNOS gene expression and the relationship with the production of inflammatory mediators in the early sepsis model induced by cecal ligation and puncture (CLP).
METHODS
Male Sprague-Dawley rats were operated on by sing the CLP method to induce of peritonitis; and then, they were sacrificed and samples of blood and lung tissues were obtained at various times (1,2,3,6,9 and 12 h after CLP). We observed the expression of iNOS mRNA from lung tissues and measured the synthesis of nitric oxide, IL-1beta , and TNF-alpha from the blood.
RESULTS
iNOS mRNA began to be expressed at 3 h and was maintained untill 12 h after CLP. The nitric oxide concentration was increased significantly at 6 h, reached its peak level at 9 h, and maintained a plateau untill 12 h after CLP. TNF-alpha began to be detected at 3 h, increased gradually, and decreased steeply from 9 h after CLP. IL-1beta showed its peak level at 6 h after CLP, and tended to decrease without significance.
CONCLUSION
We observed that the iNOS gene was expressed later in peritonitis-induced sepsis than in LPSinduced sepsis. Nitric oxide and key inflammatory mediators were also expressed later in peritonitis-induced sepsis than in LPS-induced sepsis.
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Summary
- Effect of Heat Shock Protein 70 on Inducible Nitric Oxide Synthase during Sepsis in Rats
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Yong Keun Lee, Hyo Keun Shin, Woon Yong Kwon, Gil Joon Suh, Yeo Kyu Youn
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J Korean Soc Traumatol. 2008;21(1):59-65.
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Abstract
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- PURPOSE
The aim of this study was to evaluate the effect of overexpression of heat shock protein 70 (HSP70) on the expression of inducible nitric oxide synthase and on the concentration of nitric oxide and to determine the mechanism for the relationship between HSP70 and inducible nitric oxide synthase (iNOS) in sepsis.
METHODS
Experiments were performed on male Sprague-Dawley rats, and sepsis was induced by using cecal ligation and puncture (CLP). Glutamine (GLN) or saline was administered 1 h after initiation of sepsis. We acquired serum and lung tissues from the rats 12 h or 24 h after initiation of sepsis. We analyzed the concentration of nitric oxide, the expression of HSP70 in the lung, and the gene expression of iNOS in the lung.
RESULTS
In CLP+GLN, glutamine given after initiation of sepsis enhanced the expression of HSP70 in the lung at 12 h (CLP+GLN vs. CLP:: 47.19 +/- 10.04 vs. 33.22 +/- 8.28, p = 0.025) and 24 h (CLP+GLN vs. CLP: 47.06 +/- 10.60 vs. 31.90 +/- 4.83, p = 0.004). In CLP+GLN, glutamine attenuated the expression of iNOS mRNA in the lung at 12 h (CLP+GLN vs. CLP: 4167.17 +/- 951.59 vs. 5513.73 +/- 1051.60, p = 0.025) and 24 h (CLP+GLN vs. CLP: 9,437.65 +/- 2,521.07 vs. 18,740.27 +/- 8,241.20, p = 0.016) and reduced the concentration of nitric oxide in serum at 12 h (CLP+GLN vs. CLP: 0.86 +/- 0.48 vs. 3.82 +/- 2.53 micromol/L, p = 0.016) and 24 h (CLP+GLN vs. CLP: 0.39 +/- 0.25 vs. 1.85 +/- 1.70 micromol/L, p = 0.025).
CONCLUSION
The overexpression of HSP70 induced by the administration of glutamine in sepsis attenuated the gene expression of iNOS and reduced the concentration of nitric oxide.
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Summary
- The Effect of Hypothermia on Lung Inducible Nitric Oxide Synthase Gene Expression in Intestinal Ischemia-Reperfusion Injury
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Kyuseok Kim, Jeong Hun Lee, Gil Joon Suh, Yeo Kyu Youn, Young Joon Kang, Min A Kim, Sang Ki Cho, Hyo Keun Shin
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J Korean Soc Traumatol. 2006;19(1):14-20.
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Abstract
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- PURPOSE
Although hypothermia has been used in many clinical situations, such as post cardiopulmonary resuscitation, stroke, traumatic brain injury, septic shock, and hemorrhagic shock, the mechanism by which it works has not been clearly elucidated. We aimed to evaluate the effect of hypothermia on the plasma nitric oxide (NO) concentration, lung iNOS expression, and histologic changes in intestinal ischemia-reperfusion (IR).
METHOD
Male Sprague-Dawley rats were randomly divided into the hypothermia group (HT, n=8, 27~30 degrees C) and the normothermia group (NT, n=8, 36~37 degrees C). They underwent 30 min of intestinal ischemia by clamping the superior mesenteric artery, which was followed by 1.5 h of reperfusion. They were then sacrificed. The acute lung injury (ALI) score, the plasma NO concentration, and lung iNOS gene expression were measured.
RESULTS
Compared with the HT group, the NT group showed severe infiltrations of inflammatrory cells, alveolar hemorrhages, and interstitial hypertrophies in lung tissues. There were significant differences in the ALI scores between the NT and the HT groups (8.7 +/- 1.5/HPF in NT vs 5.8 +/- 1.2/HPF in HT, p=0.008). Although the plasma NO concentration was slightly lower in the HT group, there was no significant difference between the two groups (0.80 +/- 0.24 micromol/L in NT vs 0.75 +/- 0.30 micromol/L in HT, p=0.917). Lung iNOS gene expression was stronger in the NT group than in the HT group. The band density of the expression of iNOS in lung tissues was significantly increased in the NT group compared to the HT group (5.54 +/- 2.75 in NT vs 0.08 +/- 0.52 in HT, p=0.002).
CONCLUSIONS
This study showed that hypothermia in intestinal IR reduces inflammatory responses, ALI scores, and iNOS gene expression in lung tissues. There was no significant effect of hypothermia on the plasma NO concentration.
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Summary
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