Ameliorative effect of atractylenolide III in the mast cell proliferation induced by TSLP

Yoou, Myoung-schook; Nam, Sun‐Young; Jin, Mu Hyun; Lee, So Young; Kim, Mi-Sun; Roh, Seok Seon; Choi, In Hwa; Woo, Nariyah; Lim, Seokwon; Kim, Dong Hyun; Jang, Jae-Bum; Kim, Hyung-Min; Jeong, Hyun‐Ja

doi:10.1016/j.fct.2017.05.042

Cited by 23 publications

(15 citation statements)

References 41 publications

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“…A study carried out by Miossec et al [37] demonstrated that caspase-3 precursor is massively cleaved into its active form during T-lymphocyte proliferation without inducing any form of cell death. In our previous study, we showed that actractylenolide III increased caspase-3 activation decreased by TSLP, but it did not affect apoptosis [38]. Chen et al [39] reported that rutin induced cell cycle arrest and induced apoptosis of neuroblastoma by modulating the expression of apoptotic proteins.…”

Section: Discussionmentioning

confidence: 88%

The new therapeutic herbal drug HM0601 and its bioactive compound rutin exert potent antiproliferative activities in mast cells

Jeong

Yoou

Han

et al. 2018

Fundamemntal Clinical Pharma

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HM0601 consists of Allium hookeri and Lycium chinense fruit and contains a lot of rutin. Here, we ascertained whether HM0601 and its major compound rutin reduce proliferation of human mast cell line, HMC-1, under thymic stromal lymphopoietin (TSLP) stimulation. Therapeutic rutin or HM0601 treatment considerably reduced proliferation of mast cells without exposing activated HMC-1 cells to any cytotoxicity. Reduced levels of mouse double minute 2 and phosphorylated signal transducers and activators of transcription 6 were accompanied by treatment with rutin or HM0601. In TSLP-stimulated cells, rutin or HM0601 treatment significantly impaired levels of interleukin (IL)-13 and Bcl2 expression. Notably, rutin or HM0601 treatment returned Bax and phosphorylated p53 protein levels and caspase-3 activities impaired by TSLP. In addition, levels of inflammatory cytokine were considerably reduced by treatment with rutin or HM0601 on TSLP-stimulated cells. In conclusion, these results indicate that HM0601 can be used as a new therapeutic herbal drug for prevention and therapeutic intervention of allergic inflammatory diseases.

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Section: Discussionmentioning

confidence: 88%

The new therapeutic herbal drug HM0601 and its bioactive compound rutin exert potent antiproliferative activities in mast cells

Jeong

Yoou

Han

et al. 2018

Fundamemntal Clinical Pharma

Self Cite

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“…The pervious literatures showed that ATLI, ATLII, and ATLIII display potential to regulate antiinflammatory immune responses (Wang et al, 2009). It was also reported that ATLIII inhibits mast cell proliferation, upregulates antiinflammatory cytokines (Yoou et al, 2017), and inhibits proinflammatory cytokines such as IL-6, IL-8, IL-1b, and TNF-a in tumor microenvironment. ATLIII also inhibits NF-kB and MAPK pathway activation in cancer (Ji et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

The Anticancer Effects of Atractylenolide III Associate With the Downregulation of Jak3/Stat3-Dependent IDO Expression

et al. 2020

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Objective: Indoleamin-2,3-dioxygenase-1 (IDO) has been identified as a checkpoint protein involved in generating the immunosuppressive tumor microenvironment that supports tumor growth. It has been reported that atractylenolide III (ATLIII) has anticancer and immune modulatory effects. This study is to determine the anticancer effects of ATLIII with the Jak3/Stat3-dependent IDO inactivation. Methods:We assessed the cytotoxicity of ATLIII and IFN-g on lung cancer cells by MTT. We determined the efficacy of ATLIII on IFN-g-induced IDO expression by RT-PCR and Western blot. We also determined the efficacy of ATLIII on Jak3/Stat3 pathway expression induced by IFN-g and Jak3/Stat3-dependent IDO activation. Further molecular docking assay predicted the binding activity and site of ATLIII to Jak3 protein. Additional immunofluorescence staining was used to measure the Stat3 intracellular localization. Finally, we performed mouse animal experiments to observe changes in the expression of IDO, p-Jak3, p-Stat3, and tryptophan/kynurenine after ATLIII administration.Results: ATLIII showed no cytotoxicity at a wide of dosage range. ATLIII reduced the phosphorylation level of Jak3 and Stat3 in response to IFN-g stimulation, then remarkably reduced the nuclear translocation of p-Stat3 by IFN-g. Lastly, ATLIII significantly downregulated the expression level of IDO at a wide dosage range. Molecular docking assay showed that the oxygen atom on the five-membered ring of ATLIII was capable of forming a hydrogen bond with Leu905-NH2 site of Jak3 protein. Further evidence showed that though IFN-g had normal capacity to trigger Stat3 phosphorylation, nuclear translocation, and promoter luciferase activity, ATLIII failed to trigger efficacy on reducing these changes under forced Jak3-Leu905 mutant expression condition. Finally, we confirmed this view in in vivo experiments.Conclusion: ATLIII has shown significant efficacy to inhibit IFN-g-triggered Jak3/Stat3 pathway-dependent IDO activation, and do so through a direct binding to Jak3 protein.This study elucidated a new mechanism for the anticancer effect of ATLIII, which may provide a feasible target for the clinical immunotherapy of malignant tumors.

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“…Meanwhile, a former research revealed that alisol C monoacetate and alisol B could inhibit LPS-induced inflammatory reaction [ 61 ]. Although it is unclear whether atractylenolide can improve NAFLD, it has a definite anti-inflammatory and antiapoptosis effect [ 62 , 63 ]. Due to complicated components of Chinese herbal medicine, we only identified ten of the main components of DZD.…”

Section: Discussionmentioning

confidence: 99%

Dahuang Zexie Decoction Protects against High‐Fat Diet‐Induced NAFLD by Modulating Gut Microbiota‐Mediated Toll‐Like Receptor 4 Signaling Activation and Loss of Intestinal Barrier

Fang

Sun

Xue

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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Increasing evidence suggests that intestinal dysbiosis, intestinal barrier dysfunction, and activated Toll-like receptor 4 (TLR4) signaling play key roles in the pathogenesis of NAFLD. Dahuang Zexie Decoction (DZD) has been verified to be effective for treating NAFLD, but the mechanisms remain unclear. In this study, we investigated the effects of DZD on NAFLD rats and determined whether such effects were associated with change of the gut microbiota, downregulated activity of the TLR4 signaling pathway, and increased expressions of tight junction (TJ) proteins in the gut. Male Sprague Dawley rats were fed high-fat diet (HFD) for 16 weeks to induce NAFLD and then given DZD intervention for 4 weeks. We found that DZD reduced body and liver weights of NAFLD rats, improved serum lipid levels and liver function parameters, and relieved NAFLD. We further found that DZD changed intestinal bacterial communities, inhibited the intestinal TLR4 signaling pathway, and restored the expressions of TJ proteins in the gut. Meanwhile ten potential components of DZD had been identified. These findings suggest that DZD may protects against NAFLD by modulating gut microbiota-mediated TLR4 signaling activation and loss of intestinal barrier. However, further studies are needed to clarify the mechanism by which DZD treats NAFLD.

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Ameliorative effect of atractylenolide III in the mast cell proliferation induced by TSLP

Cited by 23 publications

References 41 publications

The new therapeutic herbal drug HM0601 and its bioactive compound rutin exert potent antiproliferative activities in mast cells

The new therapeutic herbal drug HM0601 and its bioactive compound rutin exert potent antiproliferative activities in mast cells

The Anticancer Effects of Atractylenolide III Associate With the Downregulation of Jak3/Stat3-Dependent IDO Expression

Dahuang Zexie Decoction Protects against High‐Fat Diet‐Induced NAFLD by Modulating Gut Microbiota‐Mediated Toll‐Like Receptor 4 Signaling Activation and Loss of Intestinal Barrier

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