“…Meanwhile, the NF-κB and MAPK pathways can be activated by phosphorylation and translocation of NF-κB and AP-1 subunits, respectively [ 67 , 68 ]. Both transcription factors upregulate pro-inflammatory cytokines, including TNF-α, interleukin-1 beta (IL-1β), IL-6, COX-2, and inducible NO synthase (iNOS) [ 69 , 70 , 71 ]. Interestingly, it has been reported that dietary lignans and their metabolites derived from gut microbiota control the inflammatory response through suppression of these pathways [ 72 , 73 ].…”
Section: Anti-inflammatory Properties Of Lignansmentioning
Since chronic inflammation can be seen in severe, long-lasting diseases such as cancer, there is a high demand for effective methods to modulate inflammatory responses. Among many therapeutic candidates, lignans, absorbed from various plant sources, represent a type of phytoestrogen classified into secoisolariciresionol (Seco), pinoresinol (Pino), matairesinol (Mat), medioresinol (Med), sesamin (Ses), syringaresinol (Syr), and lariciresinol (Lari). Lignans consumed by humans can be further modified into END or ENL by the activities of gut microbiota. Lignans are known to exert antioxidant and anti-inflammatory activities, together with activity in estrogen receptor-dependent pathways. Lignans may have therapeutic potential for postmenopausal symptoms, including cardiovascular disease, osteoporosis, and psychological disorders. Moreover, the antitumor efficacy of lignans has been demonstrated in various cancer cell lines, including hormone-dependent breast cancer and prostate cancer, as well as colorectal cancer. Interestingly, the molecular mechanisms of lignans in these diseases involve the inhibition of inflammatory signals, including the nuclear factor (NF)-κB pathway. Therefore, we summarize the recent in vitro and in vivo studies evaluating the biological effects of various lignans, focusing on their values as effective anti-inflammatory agents.
“…Meanwhile, the NF-κB and MAPK pathways can be activated by phosphorylation and translocation of NF-κB and AP-1 subunits, respectively [ 67 , 68 ]. Both transcription factors upregulate pro-inflammatory cytokines, including TNF-α, interleukin-1 beta (IL-1β), IL-6, COX-2, and inducible NO synthase (iNOS) [ 69 , 70 , 71 ]. Interestingly, it has been reported that dietary lignans and their metabolites derived from gut microbiota control the inflammatory response through suppression of these pathways [ 72 , 73 ].…”
Section: Anti-inflammatory Properties Of Lignansmentioning
Since chronic inflammation can be seen in severe, long-lasting diseases such as cancer, there is a high demand for effective methods to modulate inflammatory responses. Among many therapeutic candidates, lignans, absorbed from various plant sources, represent a type of phytoestrogen classified into secoisolariciresionol (Seco), pinoresinol (Pino), matairesinol (Mat), medioresinol (Med), sesamin (Ses), syringaresinol (Syr), and lariciresinol (Lari). Lignans consumed by humans can be further modified into END or ENL by the activities of gut microbiota. Lignans are known to exert antioxidant and anti-inflammatory activities, together with activity in estrogen receptor-dependent pathways. Lignans may have therapeutic potential for postmenopausal symptoms, including cardiovascular disease, osteoporosis, and psychological disorders. Moreover, the antitumor efficacy of lignans has been demonstrated in various cancer cell lines, including hormone-dependent breast cancer and prostate cancer, as well as colorectal cancer. Interestingly, the molecular mechanisms of lignans in these diseases involve the inhibition of inflammatory signals, including the nuclear factor (NF)-κB pathway. Therefore, we summarize the recent in vitro and in vivo studies evaluating the biological effects of various lignans, focusing on their values as effective anti-inflammatory agents.
“…Callerya atropurpurea (family: Fabaceae, genus: Adinobortys) belongs to the Callerya clade, and it is also known as Adinobotrys atropurpures . C. atropurpurea a tropical fruit tree species that inhabits Laos, Malaysia, Thailand, and Vietnam [ 29 , 30 , 31 , 32 ]. In the past, the local people used the twigs and roots of C. atropurpurea to stupefy fish and kill insects [ 29 ].…”
Section: Introductionmentioning
confidence: 99%
“…In the past, the local people used the twigs and roots of C. atropurpurea to stupefy fish and kill insects [ 29 ]. The anti-inflammatory effects of C. atropurpurea have been reported [ 31 ]. In this paper, it was found that Ca-EE can significantly suppress lipopolysaccharide-triggered nitric oxide production without exhibiting cytotoxicity [ 31 ].…”
Section: Introductionmentioning
confidence: 99%
“…The anti-inflammatory effects of C. atropurpurea have been reported [ 31 ]. In this paper, it was found that Ca-EE can significantly suppress lipopolysaccharide-triggered nitric oxide production without exhibiting cytotoxicity [ 31 ]. In addition, this extract reduced TLR4 expression, changed MyD88/TRAF6 interaction, and altered the phospho-Src/PI3K/AKT and phosphor-MAPK pathways [ 31 ].…”
Section: Introductionmentioning
confidence: 99%
“…In this paper, it was found that Ca-EE can significantly suppress lipopolysaccharide-triggered nitric oxide production without exhibiting cytotoxicity [ 31 ]. In addition, this extract reduced TLR4 expression, changed MyD88/TRAF6 interaction, and altered the phospho-Src/PI3K/AKT and phosphor-MAPK pathways [ 31 ]. Under in vivo investigation, Ca-EE was revealed to reduce HCl/EtOH-induced gastric ulcer and LPS/poly (I:C)-induced septic shock [ 31 ].…”
(1) Background: Callerya atropurpurea is found in Laos, Thailand, and Vietnam. Although the anti-inflammatory action of C. atropurpurea has been investigated, the functions of this plant in allergic responses are not understood. Here, we explored the antiallergic mechanism of C. atropurpurea ethanol extract (Ca-EE) using in vitro assays and an in vivo atopic model. (2) Methods: The constituents of Ca-EE were analyzed using GC/MS. Inhibition of lipoxygenase and β-hexosaminidase activity was examined, and the expression of inflammatory genes was measured by quantitative real-time PCR. The regulatory roles of Ca-EE in IgE/FcεRI signaling were examined by Western blotting. The DNCB-induced atopic dermatitis mouse model was performed with histological analysis. (3) Results: Ca-EE comprised cis-raphasatin, lupeol, some sugars, and fatty acids. In RBL-2H3 cells, treatment with Ca-EE significantly reduced the activities of lipoxygenase and β-hexosaminidase, as well as cytokine gene expression. IgE-mediated signaling was downregulated by blocking Lyn kinases. Moreover, Ca-EE effectively inhibited allergic symptoms in the DNCB-induced atopic dermatitis model without toxicity. (4) Conclusions: Ca-EE displayed antiallergic activities through regulating IgE/Lyn signaling in RBL-2H3 cells and a contact dermatitis model. These results indicate that Ca-EE could be effective for allergic disease treatment.
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