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Luteolin-Peanut Shell can be anti-inflammatory?

Date:2019-10-28    Views:57

Anti-inflammatory

The anti-inflammatory activity of Luteolin is mainly shown in its ability to reduce the activity of inflammatory factor transcriptional regulators and reduce the production of pro-inflammatory cytokines and inflammatory mediators. Chen et al found that pretreatment with Luteolin reduced the pro-inflammatory factor tumor necrosis factor-α (TNF-α) produced by reduce lipopolysaccharide (LPS)-stimulated mouse alveolar macrophage MH-S cells interleukin-6 (IL-6) and mediators of inflammation nitric oxide (NO)prostaglandin E2 (PGE2), RT-PCR results show that Luteolin is at mRNA level the expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) was inhibited. Further studies have shown that the mechanism of the above phenomenon is that Luteolin reduces the activity of nuclear factor-kappa B (NF-κB), inhibits its DNA-binding activity, and blocks the nuclear translocation of NF-κB P65. At the same time, Luteolin also reduced the activity of activating protein-1 (AP-1) and decreased its DNA binding activity. Luteolin exerts an anti-inflammatory effect by inhibiting both NF-κB and AP-1 pathways. Luteolin can also inhibit palmitate-induced NF-κB inhibitory protein (inhibitor of NF-κB, IκB) α NF-κB inhibitory factor kinase β (NF-κB inhibitory cofactor kinase β, IKKβ) in human umbilical vein endothelial cells phosphorylation inhibits NF-κB activation and reduces inflammation, thereby reducing insulin resistance.

Toll-like receptors (TLRs) are one of the cellular transmembrane receptors and pathogen pattern recognition receptors in the innate immune system, which can pass the interferon-β TIR domain-containing adaptor inducing interferon-β, TRIF dependent signaling pathway triggers an inflammatory response and plays an important role in acute inflammatory responses. Lee et al first treated the cells with Luteolin, then stimulated the cells with the TLR3 agonist poly (I:C) and the TLR4 agonist LPS respectively, and found that Luteolin significantly reduced the TLR target genes TNF-α, IL-6, IL- 12, IL-27, chemotactic factor IP-10 (interferon-inducible protein-10), interferon-β, IFNβ) and chemokine (CXC motif) ligand 9, CXCL9) chemokine expression. Moreover, Luteolin inhibited the activation of downstream interferon regulatory factor 3 (IRF3) and NF-κB in cells with persistent expression of TLR4 and TRIF. These all reflect the inhibitory effect of Luteolin on TLR3 and TLR4 activity. TANK-binding kinase 1 (TBK1) make the IRF3 phosphorylates and activates IRF3. Research has shown that Luteolin can inhibit TBK1 kinase activity in a dose-dependent manner. Luteolin reduces inflammation by inhibiting TRIF-dependent Toll-like receptor signaling.


Carrageenan is a sulfated polysaccharide that triggers an inflammatory response by activating NF-κB. In vivo experiments showed that pretreatment of 50 mg/kg Luteolin significantly inhibited carrageenan-induced paw edema. Luteolin also inhibited mouse granuloma and balloon swelling, and inhibited the proliferation of mouse spleen cells induced by concanavalin A in a concentration-dependent manner. Further research indicated that these may be related to the inhibition of COX-2 activity by Luteolin.

 

The research result proved Luteolin has both anti-inflammatory activity in vitro and in vivo. 


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