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[Effect of heparin upon inflammatory reaction of endotoxin-induced acute lung injury in rat].
Zhonghua Yi Xue Za Zhi 2009; 89(38):2722-5ZY

Abstract

OBJECTIVE

To investigate the effects of heparin upon inflammatory reaction and associated mechanism of endotoxin-induced acute lung injury (ALI) in rat.

METHODS

Thirty-six male Sprague-Dawley rats were randomly divided into three equal groups namely: ALI group, heparin treatment group and normal control group. The ALI rats were induced by injecting endotoxin intravenously and sacrificed at 4 h after model establishment. The lung histology was scored by a modification of Smith technique. The albumin permeability of pulmonary microvascular (P(alb)) was measured by single nuclide tracer technique. Tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6) and von Willebrand factor (vWF) levels of serum were determined using commercial enzyme-linked immunosorbent assay kits. The expressions of lung tissue extacellular signal-regulated kinases (ERK)-1/2, P38 mitogen-activated protein kinase (MAPK) and c-jun N-terminal kinases (JNK) were determined by Western blotting.

RESULTS

The Smith lung injury score in heparin treatment group and ALI group were (5.00 +/- 1.26) and (8.00 +/- 1.09) respectively. The values were significantly higher than that of normal control group (0.67 +/- 0.52, both P < 0.01). However, the Smith lung injury score in heparin treatment group was significantly lower than that of ALI group (P < 0.01). The P(alb), TNF-alpha, IL-6 and vWF of heparin treatment group were (0.28 +/- 0.04), (1.92 +/- 0.35) microg/L, (1.22 +/- 0.13) ng/ml and (24.9 +/- 4.0) U/L respectively. The values were significantly higher than those of normal control group [0.20 +/- 0.02, (0.51 +/- 0.09) microg/L, (0.23 +/- 0.05) ng/ml and (14.0 +/- 3.0) U/L respectively, all P < 0.01] but significantly lower than those of ALI group [(0.38 +/- 0.04), (2.77 +/- 0.37) microg/L, (1.62 +/- 0.13) ng/ml and (31.8 +/- 7.5) U/L respectively, all P < 0.01]. The lung tissue levels of phospho-ERK1/2 and phospho-P38 MAPK expressions of heparin treatment group were markedly higher than those of normal control group, whereas markedly lower than those of ALI group. There was no marked difference of phospho-JNK expression in all three groups.

CONCLUSION

Heparin markedly inhibits the expressions of phospho-ERK1/2 and phospho-P38 MAPK, down-regulates the inflammatory reaction, attenuates the endothelial permeability of pulmonary vasculature and significantly improves endotoxin-induced lung injury in rats.

Authors+Show Affiliations

Department of Respiratory Diseases, Clinical School of Nanjing University, Nanjing General Hospital of Nanjing Military Command, Nanjing 210002, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article
Research Support, Non-U.S. Gov't

Language

chi

PubMed ID

20137277

Citation

Sun, Hui-Ming, et al. "[Effect of Heparin Upon Inflammatory Reaction of Endotoxin-induced Acute Lung Injury in Rat]." Zhonghua Yi Xue Za Zhi, vol. 89, no. 38, 2009, pp. 2722-5.
Sun HM, Shi Y, Song Y, et al. [Effect of heparin upon inflammatory reaction of endotoxin-induced acute lung injury in rat]. Zhonghua Yi Xue Za Zhi. 2009;89(38):2722-5.
Sun, H. M., Shi, Y., Song, Y., Lin, X. Q., Shen, X. K., & Hong, L. Z. (2009). [Effect of heparin upon inflammatory reaction of endotoxin-induced acute lung injury in rat]. Zhonghua Yi Xue Za Zhi, 89(38), pp. 2722-5.
Sun HM, et al. [Effect of Heparin Upon Inflammatory Reaction of Endotoxin-induced Acute Lung Injury in Rat]. Zhonghua Yi Xue Za Zhi. 2009 Oct 20;89(38):2722-5. PubMed PMID: 20137277.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Effect of heparin upon inflammatory reaction of endotoxin-induced acute lung injury in rat]. AU - Sun,Hui-Ming, AU - Shi,Yi, AU - Song,Yong, AU - Lin,Xin-Qing, AU - Shen,Xiao-Kun, AU - Hong,Ling-Zhi, PY - 2010/2/9/entrez PY - 2010/2/9/pubmed PY - 2010/6/9/medline SP - 2722 EP - 5 JF - Zhonghua yi xue za zhi JO - Zhonghua Yi Xue Za Zhi VL - 89 IS - 38 N2 - OBJECTIVE: To investigate the effects of heparin upon inflammatory reaction and associated mechanism of endotoxin-induced acute lung injury (ALI) in rat. METHODS: Thirty-six male Sprague-Dawley rats were randomly divided into three equal groups namely: ALI group, heparin treatment group and normal control group. The ALI rats were induced by injecting endotoxin intravenously and sacrificed at 4 h after model establishment. The lung histology was scored by a modification of Smith technique. The albumin permeability of pulmonary microvascular (P(alb)) was measured by single nuclide tracer technique. Tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6) and von Willebrand factor (vWF) levels of serum were determined using commercial enzyme-linked immunosorbent assay kits. The expressions of lung tissue extacellular signal-regulated kinases (ERK)-1/2, P38 mitogen-activated protein kinase (MAPK) and c-jun N-terminal kinases (JNK) were determined by Western blotting. RESULTS: The Smith lung injury score in heparin treatment group and ALI group were (5.00 +/- 1.26) and (8.00 +/- 1.09) respectively. The values were significantly higher than that of normal control group (0.67 +/- 0.52, both P < 0.01). However, the Smith lung injury score in heparin treatment group was significantly lower than that of ALI group (P < 0.01). The P(alb), TNF-alpha, IL-6 and vWF of heparin treatment group were (0.28 +/- 0.04), (1.92 +/- 0.35) microg/L, (1.22 +/- 0.13) ng/ml and (24.9 +/- 4.0) U/L respectively. The values were significantly higher than those of normal control group [0.20 +/- 0.02, (0.51 +/- 0.09) microg/L, (0.23 +/- 0.05) ng/ml and (14.0 +/- 3.0) U/L respectively, all P < 0.01] but significantly lower than those of ALI group [(0.38 +/- 0.04), (2.77 +/- 0.37) microg/L, (1.62 +/- 0.13) ng/ml and (31.8 +/- 7.5) U/L respectively, all P < 0.01]. The lung tissue levels of phospho-ERK1/2 and phospho-P38 MAPK expressions of heparin treatment group were markedly higher than those of normal control group, whereas markedly lower than those of ALI group. There was no marked difference of phospho-JNK expression in all three groups. CONCLUSION: Heparin markedly inhibits the expressions of phospho-ERK1/2 and phospho-P38 MAPK, down-regulates the inflammatory reaction, attenuates the endothelial permeability of pulmonary vasculature and significantly improves endotoxin-induced lung injury in rats. SN - 0376-2491 UR - https://www.unboundmedicine.com/medline/citation/20137277/[Effect_of_heparin_upon_inflammatory_reaction_of_endotoxin_induced_acute_lung_injury_in_rat]_ L2 - http://journal.yiigle.com/LinkIn.do?linkin_type=pubmed&amp;issn=0376-2491&amp;year=2009&amp;vol=89&amp;issue=38&amp;fpage=2722 DB - PRIME DP - Unbound Medicine ER -