Abstract | PURPOSE: METHODS: RESULTS: Histological examination revealed that interstitial edema, leukocytic infiltration, and HMGB1 protein expression were markedly reduced in the NM+LPS group compared to the LPS group. Furthermore, the LPS-induced increases in PAI-1 activity and in plasma TNF-alpha concentrations were also lower in the rats given both NM and LPS than in the rats given LPS alone. CONCLUSIONS: The anticoagulatory activity of NM may have inhibited PAI-1, while its anti-inflammatory activity blockaded TNF-alpha, thereby indirectly inhibiting HMGB1 and reducing tissue damage in the lung. These findings indicate that NM can inhibit the lung injury induced by LPS in rats. NM is an excellent candidate for use in new therapeutic strategies to prevent or minimize lung injury.
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Authors | Satoshi Hagiwara, Hideo Iwasaka, Takayuki Noguchi |
Journal | Journal of anesthesia
(J Anesth)
Vol. 21
Issue 2
Pg. 164-70
( 2007)
ISSN: 0913-8668 [Print] Japan |
PMID | 17458645
(Publication Type: Journal Article, Retracted Publication)
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Chemical References |
- Anti-Inflammatory Agents, Non-Steroidal
- Benzamidines
- Guanidines
- HMGB1 Protein
- Lipopolysaccharides
- Plasminogen Activator Inhibitor 1
- Tumor Necrosis Factor-alpha
- nafamostat
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Topics |
- Animals
- Anti-Inflammatory Agents, Non-Steroidal
(therapeutic use)
- Benzamidines
- Disease Models, Animal
- Guanidines
(therapeutic use)
- HMGB1 Protein
(biosynthesis, drug effects)
- Kinetics
- Lipopolysaccharides
(toxicity)
- Lung
(drug effects, pathology)
- Male
- Plasminogen Activator Inhibitor 1
(metabolism)
- Rats
- Rats, Wistar
- Respiratory Distress Syndrome
(drug therapy, physiopathology)
- Tumor Necrosis Factor-alpha
(blood, metabolism)
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