Nardochinoid B Inhibited the Activation of RAW264.7 Macrophages Stimulated by Lipopolysaccharide through Activating the Nrf2/HO-1 Pathway.
Yun-Da YaoXiu-Yu ShenJorge MachadoJin-Fang LuoYi DaiChon-Kit LioYang YuYing XiePei LuoJian-Xin LiuXin-Sheng YaoZhong-Qiu LiuHua ZhouPublished in: Molecules (Basel, Switzerland) (2019)
Nardochinoid B (NAB) is a new compound isolated from Nardostachys chinensis. Although our previous study reported that the NAB suppressed the production of nitric oxide (NO) in lipopolysaccharide (LPS)-activated RAW264.7 cells, the specific mechanisms of anti-inflammatory action of NAB remains unknown. Thus, we examined the effects of NAB against LPS-induced inflammation. In this study, we found that NAB suppressed the LPS-induced inflammatory responses by restraining the expression of inducible nitric oxide synthase (iNOS) proteins and mRNA instead of cyclooxygenase-2 (COX-2) protein and mRNA in RAW264.7 cells, implying that NAB may have lower side effects compared with nonsteroidal anti-inflammatory drugs (NSAIDs). Besides, NAB upregulated the protein and mRNA expressions of heme oxygenase (HO)-1 when it exerted its anti-inflammatory effects. Also, NAB restrained the production of NO by increasing HO-1 expression in LPS-stimulated RAW264.7 cells. Thus, it is considered that the anti-inflammatory effect of NAB is associated with an induction of antioxidant protein HO-1, and thus NAB may be a potential HO-1 inducer for treating inflammatory diseases. Moreover, our study found that the inhibitory effect of NAB on NO is similar to that of the positive drug dexamethasone, suggesting that NAB has great potential for developing new drugs in treating inflammatory diseases.
Keyphrases
- advanced non small cell lung cancer
- lps induced
- inflammatory response
- anti inflammatory
- nitric oxide
- nitric oxide synthase
- induced apoptosis
- oxidative stress
- binding protein
- cell cycle arrest
- epidermal growth factor receptor
- poor prognosis
- toll like receptor
- low dose
- signaling pathway
- cell death
- immune response
- climate change
- amino acid
- cell proliferation
- high dose
- human health
- drug induced
- electronic health record