Astragaloside IV ameliorates allergic inflammation by inhibiting key initiating factors in the initial stage of sensitization

Bao, Kaifan; Yu, Xi; Xiao, Wei; Gui, Li-Li; Liu, Hailiang; Wang, Xiaoyu; Yu, Tao; Jiang, Guilin; Hong, Min

doi:10.1038/srep38241

Cited by 18 publications

(6 citation statements)

References 40 publications

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“…Furthermore, TNF-α- and LPS-induced inflammatory reactions may be inhibited by AS-IV treatment via the NF-kB pathway in endothelial cells [8]. Evidence from pharmacological research and clinical practice suggests that AS-IV possesses effective anti-inflammatory properties and the ability to treat infectious diseases [9, 10]. …”

Section: Introductionmentioning

confidence: 99%

Astragaloside-IV Alleviates Heat-Induced Inflammation by Inhibiting Endoplasmic Reticulum Stress and Autophagy

Dong

Zhou

Zhang

et al. 2017

Cell Physiol Biochem

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Background: Thermal injury is the main cause of pulmonary disease in stroke after burn and can be life threatening. Heat-induced inflammation is an important factor that triggers a series of induces pathological changes. However, this mechanism underlying heat-induced inflammation in thermal inhalation injury remains unclear. Studies have revealed that astragaloside-IV (AS-IV), a natural compound extracted from Astragalus membranaceus, has protective effects in inflammatory diseases. Here, we investigated whether the protective effects of AS-IV occur because of the suppression of heat-induced endoplasmic reticulum (ER) stress and excessive autophagy Methods: AS-IV was administered to Wistar rats after thermal inhalation injury and 16HBE140-cells were treated with AS-IV. TNF-α, IL-6, and IL-8 levels were determined by ELISA and real-time PCR. ER stress and autophagy were determined by western blot. Autophagic flux was measured by recording the fluorescence emission of the fusion protein mRFP-GFP-LC3 by dynamic live-cell imaging. Results: AS-IV had protective effects against heat-induced reactive oxygen species production and attenuated ER stress. AS IV alleviated heat-induced excessive autophagy in vitro and in vivo. Excessive autophagy was attenuated by the PERK inhibitor GSK2656157 and eIF2α siRNA, suggesting that heat stress-induced autophagy can activate the PERK-eIF2α pathway. Beclin 1 and Atg5 siRNAs inhibited the upregulation of the inflammatory cytokines TNF-α, IL-6, and IL-8 after heat exposure. Conclusions: Thus, AS-IV may attenuate inflammatory responses by disrupting the crosstalk between autophagy and the PERK-eIF2α pathway and may be an ideal agent for treating inflammatory pulmonary diseases.

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Section: Introductionmentioning

confidence: 99%

Astragaloside-IV Alleviates Heat-Induced Inflammation by Inhibiting Endoplasmic Reticulum Stress and Autophagy

Dong

Zhou

Zhang

et al. 2017

Cell Physiol Biochem

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“…Consistent with the previous research 33) , donepezil was found to exert potent effects on inhibition of neuroinflammation and microglial activation. Lines of evidence have revealed that AS-IV is a bioactive compound with potent anti-inflammatory properties 13)- 15) , but the effect of AS-IV on neuroinflammation and related mechanism is not well elucidated. In LPS induced BV2 and primary microglia cells, AS-IV could significantly reduce the release of inflammatory mediators through activating NRF2/HO-1 via ERK signaling pathway 34) .…”

Section: Discussionmentioning

confidence: 99%

Astragaloside IV Ameliorates Cognitive Impairment and Neuroinflammation in an Oligomeric Aβ Induced Alzheimer’s Disease Mouse Model <i>via</i> Inhibition of Microglial Activation and NADPH Oxidase Expression

Chen

Yang

Cheng

et al. 2021

Biological & Pharmaceutical Bulletin

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Microglial activation and neuroinflammation induced by amyloid β (Aβ) play pivotal roles in Alzheimer's disease (AD) pathogenesis. Astragaloside IV (AS-IV) is one of the major active compounds of the traditional Chinese medicine Astmgali Radix. It has been reported that AS-IV could protect against Aβ-induced neuroinflammation and cognitive impairment, but the underlying mechanisms need to be further clarified. In this study, the therapeutic effects of AS-IV were investigated in an oligomeric Aβ (oAβ) induced AD mice model. The effects of AS-IV on microglial activation, neuronal damage and NADPH oxidase expression were further studied. Different doses of AS-IV were administered intragastrically once a day after intracerebroventricularly oAβ injection. Results of behavioral experiments including novel object recognition (NOR) test and Morris water maze (MWM) test revealed that AS-IV administration could significantly ameliorate oAβ-induced cognitive impairment in a dose dependent manner. ELISA results showed that increased levels of ROS, TNF-α, IL-1β and IL-6 in hippocampal tissues induced by oAβ injection were remarkably inhibited after AS-IV treatment. OAβ induced microglial activation and neuronal damage was significantly suppressed in AS-IV-treated mice brain, observed in immunohistochemistry results. Furthermore, oAβ upregulated protein expression of NADPH oxidase subunits gp91phox, p47phox, p22phox and p67phox were remarkably reduced by AS-IV in western blotting assay. These results revealed that AS-IV could ameliorate oAβ-induced cognitive impairment, neuroinflammation and neuronal damage, which were possibly mediated by inhibition of microglial activation and down-regulation of NADPH oxidase protein expression. Our findings provide new insights of AS-IV for the treatment of neuroinflammation related diseases such as AD.

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“…AS-IV has been shown to be effective in relieving allergic asthma [16,17]. As a representative bioactive compound of YPFS, we reported AS-IV ameliorated allergic inflammation in sensitization stage of AD by inhibiting TSLP and IL-33 production [14]. In this study, we firstly investigated the effect of AS-IV on anti-AD recurrence.…”

Section: Discussionmentioning

confidence: 99%

“…Our previous study elucidated that YPFS attenuated recurrent allergic inflammation of AD by repairing epithelial barrier defects in remission phase [13]. Furthermore, by means of bioactive components screening, we found AS-IV as a potent bioactive component of YPFS, could ameliorate the allergic inflammation by inhibiting alarmin cytokines such as thymic stromal lymphopoietin (TSLP) and IL-33 in sensitization stage of AD [14]. However, whether AS-IV could also effectively alleviate the recurrent allergic inflammation of AD was still unknown.…”

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confidence: 98%

Astragaloside IV prophylactic administration relieves recurrent allergic atopic dermatitis

Zheng

Yu²,

Wei

et al. 2020

Preprint

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BackgroundAtopic dermatitis (AD) is a common allergic inflammatory skin disease with high relapse rates and recurring severity. However, the underlying pathogenesis of AD recurrence is still unclear. Our previous study reported Astragaloside IV (AS-IV) administration in sensitization stage ameliorated the allergic inflammation of AD. In this study, we aimed to evaluate the efficacy of AS-IV which prophylactic applied in remission phase of AD and to investigate the underlying mechanisms.MethodsThe efficacy of AS-IV with prophylactic administration in remission phase of AD was evaluated in a fluorescein isothiocyanate (FITC)-induced AD relapse (AD-Re) model. Production of IL-4, IL-5 IL-13, IFN-γin mice ear tissues, IgE in serum were measured by ELISAs. Pharmacokinetic profile of AS-IV was assessed by HPLC-MS. Protein and gene expression levels of TLRs and NF-κB were detected by WB and qRT-PCR, respectively. Results: Prophylactic administration in remission phase of AD, AS-IV attenuated ear swelling, inflammatory cell infiltration, IgE production of ear homogenates in AD-Re mice. Levels of T helper (Th)2 cytokines including IL-4, IL-5, IL-13 but not Th1 cytokine IFN-γin AD-Re mice were inhibited remarkably with AS-IV preventively treatment. In addition, a different pharmacokinetic profile of AS-IV was observed as applied in remission phase. Moreover, AS-IV prophylactic administration decreased the gene expression of NF-κB and TLR8 in AD-Re mice. Consistently, the proteins expression of TLR8, TIRAP and MyD88 in ear homogenates also reduced obviously in AS-IV treated mice. Conclusions: Our finding indicated the disordered TLR8-mediated NF-κB pathway may play an important role in the pathogenesis of AD recurrence. AS-IV prophylactic administration in remission phase could regulate TLR8-mediated NF-κB pathway to against AD recurrence. These findings further improved our understanding of the pathogenesis of AD recurrence and the pharmacological effects of AS-IV.

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Astragaloside IV ameliorates allergic inflammation by inhibiting key initiating factors in the initial stage of sensitization

Cited by 18 publications

References 40 publications

Astragaloside-IV Alleviates Heat-Induced Inflammation by Inhibiting Endoplasmic Reticulum Stress and Autophagy

Astragaloside-IV Alleviates Heat-Induced Inflammation by Inhibiting Endoplasmic Reticulum Stress and Autophagy

Astragaloside IV Ameliorates Cognitive Impairment and Neuroinflammation in an Oligomeric Aβ Induced Alzheimer’s Disease Mouse Model <i>via</i> Inhibition of Microglial Activation and NADPH Oxidase Expression

Astragaloside IV prophylactic administration relieves recurrent allergic atopic dermatitis

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