犀角地黄汤对D-氨基半乳糖胺/脂多糖急性肝衰竭小鼠血浆中细胞因子的影响

张金良; 刘莉; 郭明; 李永光; 郭沫化; 孙俊

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武警医学 ›› 2013, Vol. 24 ›› Issue (7) : 605-607.

论著

犀角地黄汤对D-氨基半乳糖胺/脂多糖急性肝衰竭小鼠血浆中细胞因子的影响

张金良^¹,刘莉^²,郭明^³,李永光^²,郭沫化^³,孙俊^²

作者信息 +

Effect of Xijiao Dihuang decoction on plasma cytokines in D-GalN/LPS induced mouse acute hepatic failure model

ZHANG Jinliang^¹,LIU Li^²,GUO Ming^¹,LI Yongguang^²,GUO Muohua^¹,and SUN Jun^²

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文章历史 +

摘要

目的研究犀角地黄汤对D-氨基半乳糖胺(D-galactosamine，D-GalN)/脂多糖(lipopolysaccharide，LPS)小鼠急性肝衰竭模型血浆中细胞因子的影响，以探讨犀角地黄汤对该模型保护作用的部分机制。方法采用腹腔注射D-GalN/LPS建立小鼠急性肝衰竭模型。犀角地黄组应用犀角地黄汤灌胃，模型对照组用等体积双蒸水灌胃。应用流式微球技术(cytometricbeadarray，CBA)检测3h正常空白组、模型对照组、犀角地黄组小鼠血浆中细胞因子水平。结果犀角地黄汤组小鼠肿瘤坏死因子-α(tumornecrosisfactorα，TNFα)为(709.44±336.12)pg/ml，与模型对照组相比，对急性肝衰竭模型小鼠3hTNF-α无降低作用;IL-10为(994.67±589.63)pg/ml，与模型对照组相比，对3hIL-10有升高作用(P<0.05)。结论犀角地黄汤对急性肝衰竭模型有保护作用，其作用机制不在于降低TNF-α分泌水平，而是提高IL-10以抑制过强的炎性反应。

Abstract

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.

导出引用

张金良,刘莉,郭明,李永光,郭沫化,孙俊. 犀角地黄汤对D-氨基半乳糖胺/脂多糖急性肝衰竭小鼠血浆中细胞因子的影响[J]. 武警医学. 2013, 24(7): 605-607

ZHANG Jinliang,LIU Li,GUO Ming,LI Yongguang,GUO Muohua,and SUN Jun. Effect of Xijiao Dihuang decoction on plasma cytokines in D-GalN/LPS induced mouse acute hepatic failure model[J]. Medical Journal of the Chinese People Armed Police Forces. 2013, 24(7): 605-607

中图分类号： R2-031

参考文献

[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.