Objective To study the effect of Xijiao Dihuang decoction on the plasma cytokine levels of D-galactosamine (D-GalN)/lipoplysaccharides (LPS) induced acute liver failure mouse model, and to elucidate the potential mechanism responsible for the protective effect on this mouse model by Xijiao Dihuang decoction. Methods The mouse model of acute liver failure was developed by intraperitoneally injecting D-GalN/LPS. The Xijiao Dihuang group and the control group were intragastically administered with Xijiao Dihuang decoction and double distilled water, respectively. The cytokine level 3 h after treatment in each group was assayed by cytometric bead assay. Results The level of Tumor necrosis factor-α (TNF-α) in the Xijiao Dihuang group was (709.44±336.12) pg/ml. Compared with the control group, no significant TNF-α reduction was observed in the mouse model of acute liver failure 3 h after Xijiao Dihuang decoction treatment. In contrast, the level of IL-10 in Xijiao dihuang group was (994.67±589.63)pg/ml 3 h after treatment that was significantly elevated as compared with the control group (P<0.05). Conclusions Xijiao Dihuang decoction generates protective effect on the mouse model of acute liver failure. The underlying mechanism may be up-regulation of IL-10 production rather than reduction of TNF-α secretion, thereby inhibiting the enhanced proinflammatory responses.
Key words
Xijiao Dihuang Decoction /
D-galactosamine /
lipoplysaccharides /
acute hepatic failure /
tumor necrosis factor α /
IL-10 /
cytokine
{{custom_sec.title}}
{{custom_sec.title}}
{{custom_sec.content}}
References
[1] 张金良,王宪波,曾 辉.急性肝衰竭模型中医证型探讨[J].中国中西医结合杂志,2011,31(5): 659-661.
[2] Remick D G, Ward P A. Evaluation of endotoxin models for the study of sepsis [J].Shock, 2005, 24(1):7-11.
[3] Liu X Y, Robinson D, Veach R A, et al. Peptide directed suppression of a proinflammatory cytokine response[J].J Biol Chem, 2000, 275(22):16774-16778.
[4] Olleros M L,Vesin D, Fotio A L,et al. Soluble TNF, but not membrane TNF, is critical in LPS-induced hepatitis [J].J Hepatol, 2010, 53(6):1059-1068.
[5] Silverstein R. D-galactosamine lethality model: scope and limitations [J].J Endotoxin Res, 2004, 10(3):147-162.
[6] Nowak M, Gaines G C, Rosenberg J, et al. LPS-induced liver injury in D-galactosamine-sensitized mice requires secreted TNF-alpha and the TNF-p55 receptor [J].Am J Physiol Regul Integr Comp Physiol, 2000, 278(5):1202-1209.
[7] Kuhla A, Eipel C, Abshagen K, et al. Role of the perforin/granzyme cell death pathway in D-Gal/LPS-induced inflammatory liver injury [J].Am J Physiol Gastrointest Liver Physiol, 2009, 296(5): 1069-1076.
[8] Jesephs M D, Bahjar F R, Fukuzuka K, et al. Lipopolysaccharide and D-galactesamine-induced curve of the respiratory systempredicts effects of PEEP in ARDS: occlusion versus constant flow technique[J].Am J Respir Crit Care Med, 1994, 149(1):19-27.
[9] 张金良,吕新亮,王淑芳,等.犀角地黄汤对脂多糖诱导的感染小鼠血浆中细胞因子的影响[J].武警医学,2011,22(9): 770-773.
PDF(557 KB)
