The protective effect of atractylenolide I on systemic inflammation in the mouse model of sepsis created by cecal ligation and puncture

Wang, Aiming; Xiao, Zhiming; Zhou, Liping; Zhang, Juan; Li, Xiangmin; He, Qingchun

doi:10.3109/13880209.2015.1024330

Cited by 37 publications

(22 citation statements)

References 26 publications

(33 reference statements)

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“…Of note, the elevation of hippocampal IL-1β levels in mice subjected to CUMS was partly reversed by treatment with AT-I for 3 weeks. Previous studies have indicated that AT-I exhibited anti-inflammatory activity and inhibited the production of IL-1β (15,29), which is consistent with the ELISA results for IL-1β of the present study. In addition, it was previously demonstrated that IL-1β activates the neurotransmitters 5-HT and NE in the CNS (30).…”

Section: Discussionsupporting

confidence: 82%

Anti-depressant-like effect of atractylenolide I in a mouse model of depression induced by chronic unpredictable mild stress

Gao

Zhu

et al. 2017

Exp Ther Med

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Abstract. Atractylenolide I (AT-I), a major component of the rhizoma of Atractylodes macrocephala Koidz., exerts a wide range of activities. The purpose of the present study was to investigate the anti-depressant-like effect of AT-I in a mouse model of chronic unpredictable mild stress (CUMS), and to explore the possible molecular mechanism involved. It was revealed that AT-I significantly ameliorated CUMS-induced depressive-like behaviors, as evidenced by increased sucrose preference as well as shortened immobility time in the forced swimming and the tail suspension test. In addition, AT-I reduced CUMS-induced decreases in the concentrations of serotonin and norepinephrine in the hippocampus. Furthermore, AT-I inhibited the activation of the nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome as well as the concentration of the pro-inflammatory cytokine interleukin (IL)-1β in the hippocampi of mice subjected to CUMS. In conclusion, the results of the present study suggested that AT-I exerts anti-depressant-like effects in a CUMS-induced model of depression in mice, the molecular mechanism of which is associated with the inhibition of NLRP3 inflammasome activation to decrease IL-1β production.

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Section: Discussionsupporting

confidence: 82%

Anti-depressant-like effect of atractylenolide I in a mouse model of depression induced by chronic unpredictable mild stress

Gao

Zhu

et al. 2017

Exp Ther Med

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“…The occurrence of sepsis and consequent MOF is highly associated with bacteria and endotoxin translocation, which can trigger excessive inflammatory response and organ dysfunction [15]. LPS is the main components of the cell wall of Gram-negative bacteria and many studies proved that LPS could induce lethal inflammatory response, causing MOF and even death [9, 16]. Correspondingly, removal of LPS in animals was effective in treatment of sepsis [16].…”

Section: Discussionmentioning

confidence: 99%

“…LPS can promote overexpression of proinflammatory cytokines including IL-6, IL-1 β , and TNF- α , which was involved in subsequent sepsis [18, 19]. It was previously found that TNF- α played a pivotal in sepsis which could initiate systematic inflammatory response [9]. IL-6 is also associated with CLP induced sepsis, and it was reported that selective blockade of IL-6 transsignaling improves survival rate [20].…”

Section: Discussionmentioning

confidence: 99%

“…Recently, it was demonstrated in vivo and in vitro that maresin 1 can enhance inflammation resolution and show protective properties by inhibiting inflammatory response [7, 8]. During septic shock, many inflammatory mediators, such as interleukin-1 β , tumor necrosis factor- α , and interleukin-6, increased dramatically and caused tissue or organ damage [9]. Severe sepsis is frequently accompanied with acute respiratory distress syndrome (ARDS), hepatic dysfunction, and other organ failures, which lead to poor prognosis [10].…”

Section: Introductionmentioning

confidence: 99%

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Maresin 1 Mitigates Inflammatory Response and Protects Mice from Sepsis

Wang

et al. 2016

Mediators of Inflammation

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Sepsis, frequently caused by infection of bacteria, is considered as an uncontrollable systematic inflammation response syndrome (SIRS). Maresin 1 (Mar1) is a new proresolving mediator with potent anti-inflammatory effect in several animal models. However, its effect in sepsis is still not investigated. To address this question, we developed sepsis model in BALB/c mice by cecal ligation and puncture (CLP) with or without Mar1 treatment. Our data showed that Mar1 markedly improved survival rate and decreased the levels of proinflammatory cytokines in CLP mice such as interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β). Furthermore, Mar1 reduced serum level of lipopolysaccharide (LPS) and enhanced the bacteria clearance in mice sepsis model. Moreover, Mar1 attenuated lung injury and decreased level of alanine transaminase (ALT), aspartate transaminase (AST), creatinine (Cre), and blood urea nitrogen (BUN) in serum in mice after CLP surgery. Treatment with Mar1 inhibited activation of nuclear factor kappa B (NF-κb) pathway. In conclusion, Mar1 exhibited protective effect in sepsis by reducing LPS, bacteria burden in serum, inhibiting inflammation response, and improving vital organ function. The possible mechanism is partly involved in inhibition of NF-κb activation.

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“…Atractylodes macrocephula Koidz (A. macrocephula, also known as Baizhu), an important component in traditional Chinese herb medicine, have been shown to be beneficial for the treatment of variety of diseases including cancers by regulating various molecules and pathways [7-10]. Atractylenolide 1 (ATL-1), one of major bioactive compounds of Atractylodis macrocephalae, has anti-inflammatory and anti-tumor activities [8, 10-12].…”

Section: Introductionmentioning

confidence: 99%

Activation of ERK and Mutual Regulation of Stat3 and SP1 Contribute to Inhibition of PDK1 Expression by Atractylenolide-1 in Human Lung Cancer Cells

Xiao¹,

Zheng²,

Wu³

et al. 2017

Cell Physiol Biochem

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Background/Aims: Atractylodes macrocephula Koidz is an important ingredient in traditional Chinese herbs. One major bioactive compound, atractylenolide-1 (ATL-1), was reported to have anti-inflammatory and anti-tumor activities. However, the underlying molecular mechanism associated to this has not been well elucidated. Methods: Cell viability and cell cycle distribution were measured using 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) and flow cytometry assays, respectively. Western blot analysis was performed to examine the phosphorylation and protein expression of extracellular signaling-regulated kinase 1/2 (ERK1/2), signal transducer and activator of transcription 3 (Stat3), 3-phosphoinositide dependent protein kinase-1 (PDK1) and transcription factor SP1. QRT-PCR was used to examine the mRNA levels of PDK1 gene. Exogenously expressions of Stat3, PDK1 and SP1 were carried out by transient transfection assays. PDK1 promoter activity was measured by Secrete-Pair Dual Luminescence Assay Kit. A nude mice xenograft model was used to confirm the findings in vitro. Results: We showed that ATL-1 inhibited human lung cancer cell growth and induced cell cycle arrest. Furthermore, we found that ATL-1 stimulated phosphorylation of ERK1/2, inhibited phosphorylation and protein expressions of Stat3 and SP1; the latter were abrogated in the presence of MEK/ERK inhibitor PD98059. Moreover, ATL-1 reduced the protein, mRNA expression and promoter activity of PDK1. Intriguingly, exogenously expressed Stat3 and SP1 overcame ATL-1-inhibited SP1 and Stat3, and PDK1 protein expressions, respectively. Moreover, overexpression of PDK1 resisted the ATL-1-inhibited lung cancer cell growth. In consistent with the results in vitro, ATL-1 inhibited tumor growth, protein expressions of Stat3, SP1 and PDK1, and induced phosphorylation of ERK1/2 in vivo. Conclusion: In summary, our results show that ATL-1 inhibits lung cancer cell growth through activation of ERK1/2, followed by suppressing SP1 protein expression. ATL-1 also reduces phosphorylation and protein levels of Stat3. These are mutual regulation between Stat3 and SP1 proteins affected by ATL-1. This ultimately suppresses PDK1 gene expression. This study reveals a novel mechanism by which ATL-1 inhibits growth of lung cancer cells. Thus, targeting PDK1 pinpoints a potential in the lung cancer treatment.

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The protective effect of atractylenolide I on systemic inflammation in the mouse model of sepsis created by cecal ligation and puncture

Cited by 37 publications

References 26 publications

Anti-depressant-like effect of atractylenolide I in a mouse model of depression induced by chronic unpredictable mild stress

Anti-depressant-like effect of atractylenolide I in a mouse model of depression induced by chronic unpredictable mild stress

Maresin 1 Mitigates Inflammatory Response and Protects Mice from Sepsis

Activation of ERK and Mutual Regulation of Stat3 and SP1 Contribute to Inhibition of PDK1 Expression by Atractylenolide-1 in Human Lung Cancer Cells

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