Paeonol suppresses lipopolysaccharide-induced inflammatory cytokines in macrophage cells and protects mice from lethal endotoxin shock

被引：49

作者：

Chen, Na ^{[1
]}

Liu, Dianfeng ^{[2
]}

Soromou, Lanan Wassy ^{[1
]}

Sun, Jingjing ^{[1
]}

Zhong, Weiting ^{[1
]}

Guo, Weixiao ^{[1
]}

Huo, Meixia ^{[1
]}

Li, Hongyu ^{[1
]}

Guan, Shuang ^{[1
]}

Chen, Zhenwen ^{[3
]}

Feng, Haihua ^{[1
]}

机构：

[1] Jilin Univ, Coll Anim Sci & Vet Med, Changchun 130062, Peoples R China

[2] Jilin Univ, Lab Anim Ctr, Changchun 130062, Peoples R China

[3] Capital Med Univ, Sch Basic Med Sci, Dept Lab Anim Sci, Beijing 100069, Peoples R China

来源：

FUNDAMENTAL & CLINICAL PHARMACOLOGY | 2014年 / 28卷 / 03期

基金：

中国博士后科学基金;

关键词：

survival; paeonol; cytokines; pathway; lipopolysaccharide; TUMOR-NECROSIS-FACTOR; NF-KAPPA-B; INTERLEUKIN-10; LACTIFLORA; KINASE; LPS; EPIDEMIOLOGY; STIMULATION; INHIBITION; RECEPTORS;

D O I：

10.1111/fcp.12019

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Paeonol (2 '-hydroxy-4 '-methoxyacetophenone) is the main phenolic compound of the radix of Paeonia suffruticosa which has been used as traditional Chinese medicine. In this study, we primarily investigated the anti-inflammatory effects and the underlying mechanisms of paeonol in RAW macrophage cells; and based on these effects, we assessed the protective effects of paeonol on lipopolysaccharide-induced endotoxemia in mice. The in vitro study showed that paeonol regulated the production of TNF-alpha, IL-1 beta, IL-6, and IL-10 via inactivation of I kappa B alpha, ERK1/2, JNK, and p38 MAPK. In mouse model of lipopolysaccharide-induced endotoxemia, pro- and anti-inflammatory cytokines are significantly regulated, and thus the survival rates of lipolysaccharide-challenged mice are improved by paeonol (150, 200, or 250mg/kg). Therefore, paeonol has a beneficial activity against lipopolysaccharide-induced inflammation in RAW 264.7 cell and mouse models.

引用

页码：268 / 276

页数：9

共 41 条

[1] Innate immunity and toll-like receptors: Clinical implications of basic science research [J].

Abreu, MT ;

Arditi, M .

JOURNAL OF PEDIATRICS, 2004, 144 (04) :421-429

[2]

Aggarwal BB, 1996, EUR CYTOKINE NETW, V7, P93

[3] Epidemiology of severe sepsis in the United States: Analysis of incidence, outcome, and associated costs of care [J].

Angus, DC ;

Linde-Zwirble, WT ;

Lidicker, J ;

Clermont, G ;

Carcillo, J ;

Pinsky, MR .

CRITICAL CARE MEDICINE, 2001, 29 (07) :1303-1310

[4] Current epidemiology of septic shock - The CUB-Rea network [J].

Annane, D ;

Aegerter, P ;

Jars-Guincestre, MC ;

Guidet, B .

AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2003, 168 (02) :165-172

[5] INTERLEUKIN-10 IS A CENTRAL REGULATOR OF THE RESPONSE TO LPS IN MURINE MODELS OF ENDOTOXIC-SHOCK AND THE SHWARTZMAN REACTION BUT NOT ENDOTOXIN TOLERANCE [J].

BERG, DJ ;

KUHN, R ;

RAJEWSKY, K ;

MULLER, W ;

MENON, S ;

DAVIDSON, N ;

GRUNIG, G ;

RENNICK, D .

JOURNAL OF CLINICAL INVESTIGATION, 1995, 96 (05) :2339-2347

[6] Inhibition of LPS-Induced iNOS, COX-2 and Inflammatory Mediator Expression by Paeonol through the MAPKs Inactivation in RAW 264.7 Cells [J].

Chae, Hee-Sung ;

Kang, Ok-Hwa ;

Lee, Young-Seob ;

Choi, Jang-Gi ;

Oh, You-Chang ;

Jang, Hye-Jin ;

Kim, Min-San ;

Kim, Jong-Hak ;

Jeong, Seung-Il ;

Kwon, Dong-Yeul .

AMERICAN JOURNAL OF CHINESE MEDICINE, 2009, 37 (01) :181-194

[7]

Cline M J, 1970, Ser Haematol, V3, P3

[8] THE PIVOTAL ROLE OF TUMOR-NECROSIS-FACTOR-ALPHA IN THE DEVELOPMENT OF INFLAMMATORY HYPERALGESIA [J].

CUNHA, FQ ;

POOLE, S ;

LORENZETTI, BB ;

FERREIRA, SH .

BRITISH JOURNAL OF PHARMACOLOGY, 1992, 107 (03) :660-664

[9] Cornuside Suppresses Lipopolysaccharide-Induced Inflammatory Mediators by Inhibiting Nuclear Factor-Kappa B Activation in RAW 264.7 Macrophages [J].

Cuoi, Yun Ho ;

Jin, Guang Yu ;

Li, Guang Zhao ;

Yan, Guang Hai .

BIOLOGICAL & PHARMACEUTICAL BULLETIN, 2011, 34 (07) :959-966

[10]

Ertel W, 1996, ARCH SURG-CHICAGO, V131, P51

← 1 2 3 4 5 →