IL1 induced NO production in rat liver cells increased mitochondrial membrane potential.docVIP

 PAGE \* MERGEFORMAT 15 IL1 induced NO production in rat liver cells increased mitochondrial membrane potential [Abstract] Objective: To observe the in vitro cultured rat liver cells in the pro-inflammatory cytokines IL 1 stimulate the Nitric Oxide (NO) production and mitochondrial membrane potential, and to explore the relationship between the two. METHODS: In situ collagen perfusion enzyme isolated and cultured primary rat liver cells were treated with saline, lipopolysaccharide (LPS) (10 mg L-1), IL 1 (1 nmol L-1) and LPS (10 mg L -1) combined with IL 1 (1 nmol L-1) stimulate the liver cells, and were sacrificing 6,12,24,48 h after stimulation cells and supernatant, the supernatant by spectrophotometry the content of NO , the use of fluorescent probes with flow cytometry JC 1 mitochondrial membrane potential of liver cells. Results: IL 1 stimulated the increase of liver cells to produce NO reduced mitochondrial membrane potential, the two were in a time-dependent, and 24 h reached the peak; LPS on the liver cells do not directly induce the synthesis of NO effect, combined stimulation with IL 1 and no synergistic effect. Conclusion: IL 1 overproduction of NO induced by liver cells to inhibition of mitochondrial respiratory function may be inflammation of the potential stress and liver injury One of the mechanisms. [Keywords:] liver cells; mitochondria; interleukin-1; nitric oxide; membrane potential; rat Liver dysfunction is a common clinical manifestation in patients with sepsis, but also lead to sepsis patients with multiple organ dysfunction syndrome (multiple organ dysfunction syndrome, MODS) and the major cause of death [1]. In recent years, found that mitochondrial dysfunction body energy metabolism due to possible occurrence of sepsis and the development of MODS played a key role [25], sepsis liver to produce a large number of NO inhibition of mitochondrial respiratory function may be the potential damage mechanisms [6 7]. IL 1 is an early