- 作者: Bang Gee Hsu; Fwu Lin Yang; Ru Ping Lee; Tai Chu Peng; Horng Jyh Harn Hsing I.Chen
- 作者服務機構: Institute of Medical Sciences, Department of Nephrology, Division of Surgical Critical Care Unit, Department of Neuro-Medical Scientific Center and Division of Molecular Medicine, Tzu Chi General Hosital, Department of Nursing, Tzu Chi University, Hualien, Taiwan
- 中文摘要: --
- 英文摘要: Lipopolysaccharide is strongly associated with septicshock, leading to multiple organ failure. It can activatemonocytes and macrophages to release proinflammato-ry mediators such as tumor necrosis factor-α (TNF-α),interleukin-1 β(IL-1β),and nitric oxide(NO).The presentexperiments were designed to induce endotoxin shockby an intravenous injection of Klebsiella pneumoniaelipopolysaccharide(LPS, 10 mg/kg)in conscious rats.Arterial pressure and heart rate(HR)were continuouslymonitored for 48 h after LPS administration. N-Acetyl-cysteine was used to study its effects on organ damage.Biochemical substances were measured to reflect organfunctions. Biochemical factors included blood urea nitro-gen(BUN),creatinine (Cre),lactic dehydrogenase(LDH),creatine phosphokinase (CPK), aspartate transferase(GOT),alanine transferase(GPT), TNF-α, IL-1(β, methylguanidine(MG),and nitrites/nitrates. LPS caused signifi-cant increases in blood BUN,Cre, LDH,CPK, GOT, GPT,TNF-α,IL-1β,MG levels,and HR,as well as a decrease inmean arterial pressure and an elevation of nitrites/nitrates. N-Acetylcysteine suppressed the release ofTNF-α, IL-1β, and MG, but enhanced NO production.These actions ameliorate LPS-induced organ damage inconscious rats. The beneficial effects may suggest apotential chemopreventive effect of this compound insepsis prevention and treatment.
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- 英文關鍵字: --