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Post-treatment with N-acetylcysteine ameliorates endotoxin shock-induced organ damage in conscious rats.
Life Sci. 2006 Oct 19; 79(21):2010-6.LS

Abstract

N-acetylcysteine (NAC) is an antioxidant and cytoprotective agent with scavenging action against reactive oxygen species and inhibitory effects on pro-inflammatory cytokines. In a previous study, we found that pretreatment with NAC attenuated organ dysfunction and damage, reduced the production of free radicals, tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) following endotoxemia elicited by administration of lipopolysaccharide (LPS). In the present study, we tested the effects of post-treatment with NAC on the sepsis-induced change. Post-treatment imitates clinical therapeutic regimen with administration of drug after endotoxemia. Endotoxin shock was induced by intravenous injection of Klebsiella pneumoniae LPS (10 mg/kg) in conscious rats. Mean arterial pressure (MAP) and heart rate (HR) were continuously monitored for 48 h after LPS administration. NAC was given 20 min after LPS. Measurements of biochemical substances were taken to reflect organ functions. Biochemical factors included blood urea nitrogen (BUN), creatinine (Cre), lactate dehydrogenase (LDH), creatine phosphokinase (CPK), aspartate transferase (GOT), alanine transferase (GPT), TNF-alpha, interleukin-6 (IL-6), and interleukin-10 (IL-10). LPS significantly increased blood BUN, Cre, LDH, CPK, GOT, GPT, TNF-alpha, IL-6, IL-10 levels and HR, and decreased MAP. Post-treatment with NAC diminished the decrease in MAP, increased the HR, and decreased the markers of organ injury (BUN, Cre, LDH, CPK, GOT, GPT) and inflammatory biomarkers (TNF-alpha, IL-6, IL-10) after LPS. We conclude that post-treatment with NAC suppresses the release of plasma TNF-alpha, IL-6, and IL-10 in endotoxin shock, and decreases the markers of organ injury. These beneficial effects protect against LPS-induced kidney, heart and liver damage in conscious rats. The beneficial effects may suggest a potential chemopreventive effect of this compound after sepsis.

Authors+Show Affiliations

Department of Nephrology, Buddhist Tzu Chi General Hospital, Hualien, Taiwan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

16860347

Citation

Hsu, Bang-Gee, et al. "Post-treatment With N-acetylcysteine Ameliorates Endotoxin Shock-induced Organ Damage in Conscious Rats." Life Sciences, vol. 79, no. 21, 2006, pp. 2010-6.
Hsu BG, Lee RP, Yang FL, et al. Post-treatment with N-acetylcysteine ameliorates endotoxin shock-induced organ damage in conscious rats. Life Sci. 2006;79(21):2010-6.
Hsu, B. G., Lee, R. P., Yang, F. L., Harn, H. J., & Chen, H. I. (2006). Post-treatment with N-acetylcysteine ameliorates endotoxin shock-induced organ damage in conscious rats. Life Sciences, 79(21), 2010-6.
Hsu BG, et al. Post-treatment With N-acetylcysteine Ameliorates Endotoxin Shock-induced Organ Damage in Conscious Rats. Life Sci. 2006 Oct 19;79(21):2010-6. PubMed PMID: 16860347.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Post-treatment with N-acetylcysteine ameliorates endotoxin shock-induced organ damage in conscious rats. AU - Hsu,Bang-Gee, AU - Lee,Ru-Ping, AU - Yang,Fwu-Lin, AU - Harn,Horng-Jyh, AU - Chen,Hsing I, Y1 - 2006/07/01/ PY - 2006/02/14/received PY - 2006/06/06/revised PY - 2006/06/24/accepted PY - 2006/7/25/pubmed PY - 2006/12/9/medline PY - 2006/7/25/entrez SP - 2010 EP - 6 JF - Life sciences JO - Life Sci VL - 79 IS - 21 N2 - N-acetylcysteine (NAC) is an antioxidant and cytoprotective agent with scavenging action against reactive oxygen species and inhibitory effects on pro-inflammatory cytokines. In a previous study, we found that pretreatment with NAC attenuated organ dysfunction and damage, reduced the production of free radicals, tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) following endotoxemia elicited by administration of lipopolysaccharide (LPS). In the present study, we tested the effects of post-treatment with NAC on the sepsis-induced change. Post-treatment imitates clinical therapeutic regimen with administration of drug after endotoxemia. Endotoxin shock was induced by intravenous injection of Klebsiella pneumoniae LPS (10 mg/kg) in conscious rats. Mean arterial pressure (MAP) and heart rate (HR) were continuously monitored for 48 h after LPS administration. NAC was given 20 min after LPS. Measurements of biochemical substances were taken to reflect organ functions. Biochemical factors included blood urea nitrogen (BUN), creatinine (Cre), lactate dehydrogenase (LDH), creatine phosphokinase (CPK), aspartate transferase (GOT), alanine transferase (GPT), TNF-alpha, interleukin-6 (IL-6), and interleukin-10 (IL-10). LPS significantly increased blood BUN, Cre, LDH, CPK, GOT, GPT, TNF-alpha, IL-6, IL-10 levels and HR, and decreased MAP. Post-treatment with NAC diminished the decrease in MAP, increased the HR, and decreased the markers of organ injury (BUN, Cre, LDH, CPK, GOT, GPT) and inflammatory biomarkers (TNF-alpha, IL-6, IL-10) after LPS. We conclude that post-treatment with NAC suppresses the release of plasma TNF-alpha, IL-6, and IL-10 in endotoxin shock, and decreases the markers of organ injury. These beneficial effects protect against LPS-induced kidney, heart and liver damage in conscious rats. The beneficial effects may suggest a potential chemopreventive effect of this compound after sepsis. SN - 0024-3205 UR - https://www.unboundmedicine.com/medline/citation/16860347/Post_treatment_with_N_acetylcysteine_ameliorates_endotoxin_shock_induced_organ_damage_in_conscious_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0024-3205(06)00517-0 DB - PRIME DP - Unbound Medicine ER -