Modified Si-Miao-San extract inhibits the release of inflammatory mediators from lipopolysaccharide-stimulated mouse macrophages.
BACKGROUND
Modified Si-Miao-San (mSMS) is a prescription modified from Si-Miao-San which is an ancient Chinese prescription used to treat various ailments.


OBJECTIVE
Modified Si-Miao-San (mSMS) has been used for the treatment of infectious and inflammatory disorders in the clinic. This study was aimed to investigate its anti-inflammatory activity and underlying mechanism at cellular and molecular levels.


METHODS
We stimulated RAW264.7 cells with Lipopolysaccharide (LPS) and observed effects of mSMS on the release of inflammatory mediators such as: tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), NO, and relative gene expressions. Meanwhile, we also investigated the modulation of mSMS in inflammatory signal transduction mediated through extracellular signal-regulated protein kinase (ERK) and nuclear factor-kappaB (NF-kappaB) pathway.


RESULTS
Our findings demonstrated that mSMS significantly inhibited the excessive production of NO, TNF-alpha and IL-6 and the over expression of relative genes in LPS-stimulated macrophages. In addition, mSMS suppressed LPS-induced ERK1/2-phosphorylation and inhibited the activation of NF-kappaB by attenuation of I kappaB-alpha degradation.


CONCLUSIONS
Our results suggest that the anti-inflammatory properties of mSMS might result from the inhibition of inflammatory mediators, such as NO, TNF-alpha and IL-6, via suppression of ERK and NF-kappaB dependent pathways.
Fan
Jinghua
J
Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, 24 Tong Jia Xiang, Nanjing 210009, PR China.
Liu
Kang
K
Zhang
Zhongai
Z
Luo
Tianjiong
T
Xi
Zhilei
Z
Song
Junna
J
Liu
Baolin
B
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D004365:Drugs, Chinese Herbal / Q000494:pharmacology*; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism*; D015870:Gene Expression; D020672:I-kappa B Proteins / Q000378:metabolism; D007249:Inflammation / Q000188:drug therapy; D018836:Inflammation Mediators / Q000378:metabolism*; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D008070:Lipopolysaccharides; D008264:Macrophages / Q000187:drug effects*; D019684:Magnoliopsida; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism*; D009569:Nitric Oxide / Q000235:genetics / Q000378:metabolism; D010766:Phosphorylation; D015398:Signal Transduction / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
D000893:Anti-Inflammatory Agents; D004365:Drugs, Chinese Herbal; D020672:I-kappa B Proteins; D018836:Inflammation Mediators; D015850:Interleukin-6; D008070:Lipopolysaccharides; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D048049:Extracellular Signal-Regulated MAP Kinases