In vitro and in vivo experimental investigation of anti-inflammatory effects of Peucedanum japonicum aqueous extract by suppressing the LPS-induced NF-κB/MAPK JNK pathways

被引:3
|
作者
Gil, Tae-Yong [1 ,2 ]
Jin, Bo-Ram [1 ]
Lee, Jong-Hyun [3 ]
An, Hyo-Jin [1 ]
机构
[1] Kyung Hee Univ, Coll Pharm, Dept Oriental Pharmaceut Sci, Seoul 02447, South Korea
[2] Sangji Ji Univ, Coll Korean Med, Dept Pharmacol, Wonju 26339, Gangwon Do, South Korea
[3] Dongduk Womans Univ, Coll Pharm, Dept Pharm, 23-1 Wolgok Dong, Seoul 02748, South Korea
来源
AMERICAN JOURNAL OF CHINESE MEDICINE | 2022年 / 50卷 / 08期
基金
新加坡国家研究基金会;
关键词
Peucedanum japonicum; Inflammation; Macrophage; Sepsis; Cytokine; NITRIC-OXIDE SYNTHASE; DOWN-REGULATION; INFLAMMATION; ACTIVATION; CYCLOOXYGENASE-2;
D O I
10.1142/S0192415X22500926
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
Peucedanum japonicum Thunberg has been used to treat cold, cough, and inflammatory diseases in Southern and Eastern Asia. The effects of P. japonicum root aqueous extract (PJ) on lipopolysaccharide (LPS)-induced inflammation were investigated in RAW264.7 macrophages and an animal model of septic shock. Lipopolysaccharides are endotoxins that trigger excessive inflammatory responses, similar to those elicited by gramnegative bacteria. Inflammation is characterized by a primary defense system against pathogens and the onset of sundry diseases or illnesses, and macrophages are important components of the phagocytic system during inflammatory processes. The present study evaluated the effects of PJ on the production of pro-inflammatory mediators, such as nitric oxide and prostaglandin E-2, and assessed the expression of enzymes that induce the production of pro-inflammatory mediators using western blotting. We also evaluated the production and mRNA expression of pro-inflammatory cytokines using enzyme-linked immunosorbent assay and reverse transcription polymerise chain reaction, respectively. Using western blotting, we determined whether nuclear factor-kappa B (NF-kappa B) and c-Jun N-terminal kinase (JNK) are involved in the molecular mechanisms induced by PJ that suppressed LPS-induced inflammatory responses. We also found that PJ inhibited NF-kappa B and JNK pathways in macrophages and reduced LPS-induced mortality in the mouse model of septic shock by inhibiting the activation of NF-kappa B and JNK pathways that downregulated the expression of inflammatory mediators. These results indicated that PJ is an effective inflammatory suppressor.
引用
收藏
页码:2153 / 2169
页数:17
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