Echinacea polysaccharide alleviates LPS-induced lung injury via inhibiting inflammation, apoptosis and activation of the TLR4/NF-κB signal pathway

Zhang, Haihua; Lang, Wuying; Wang, Shiyong; Li, Binru; Li, Guangyu; Shi, Qiumei

doi:10.1016/j.intimp.2020.106974

Cited by 47 publications

(29 citation statements)

References 48 publications

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“…Our study demonstrated that LPS significantly upregulated the expression of TLR4, p-IKKα/β, p-IκBα, and p-NF-κB but decreased expression of IKKα/β, IκBα, and NF-κB. Other studies reported that LPS induced overexpression of NF-κB or kept constant ( Lee et al, 2020 ; Li et al, 2020 ; Zhang et al, 2020 ). To solve this inconsistent question, we tested different dosages and different stimulus times of LPS on NF-κB expression and found that the NF-κB expression was upregulated by LPS on 1 mg/kg at 4 h, 5 mg/kg at both 2 and 4 h, and 10 mg/ kg at 2 h. Meanwhile, the LPS on 2 mg/ kg at 2 h and 10 mg/ kg at 4 h significantly decreased the NF-κB expression ( Supplementary Figure S1 ).…”

Section: Discussionsupporting

confidence: 59%

Qingwenzhike Prescription Alleviates Acute Lung Injury Induced by LPS via Inhibiting TLR4/NF-kB Pathway and NLRP3 Inflammasome Activation

Zhang

Wang

et al. 2021

Front. Pharmacol.

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Background: Acute lung injury (ALI) is characterized by dysfunction of the alveolar epithelial membrane caused by acute inflammation and tissue injury. Qingwenzhike (QWZK) prescription has been demonstrated to be effective against respiratory viral infections in clinical practices, including coronavirus disease 2019 (COVID-19) infection. So far, the chemical compositions, protective effects on ALI, and possible anti-inflammatory mechanisms remain unknown.Methods: In this study, the compositions of QWZK were determined via the linear ion trap/electrostatic field orbital trap tandem high-resolution mass spectrometry (UHPLC-LTQ-Orbitrap MS). To test the protective effects of QWZK on ALI, an ALI model induced by lipopolysaccharide (LPS) in rats was used. The effects of QWZK on the LPS-induced ALI were evaluated by pathological changes and the number and classification of white blood cell (WBC) in bronchoalveolar lavage fluid (BALF). To investigate the possible underlying mechanisms, the contents of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein (MCP-1), interleukin-1β (IL-1β), interleukin-18 (IL-18), and immunoregulatory-related factors interferon-γ (IFN-γ) were detected by ELISA. Furthermore, the expression of Toll-like receptor 4 (TLR4), p-IKKα/β, IKKα, IKKβ, p-IκBα, IκBα, p-NF-κB, nuclear factor-κB (NF-κB), NOD-like receptor family pyrin domain containing 3 (NLRP3), cleaved caspase-1, pro-caspase-1, apoptosis-associated speck-like protein containing CARD (ASC), and β-actin were tested by Western blot.Results: A total of 99 compounds were identified in QWZK, including 33 flavonoids, 23 phenolic acids, 3 alkaloids, 3 coumarins, 20 triterpenoids, 5 anthraquinones, and 12 others. ALI rats induced by LPS exhibited significant increase in neutrophile, significant decrease in lymphocyte, and evidently thicker alveolar wall than control animals. QWZK reversed the changes in WBC count and alveolar wall to normal level on the model of ALI induced by LPS. ELISA results revealed that QWZK significantly reduced the overexpression of proinflammatory factors IL-6, TNF-α, MCP-1, IL-1β, IL-18, and IFN-γ induced by LPS. Western blot results demonstrated that QWZK significantly downregulated the overexpression of TLR4, p-IKKα/β, p-IκBα, p-NF-κB, NLRP3, cleaved caspase-1, and ASC induced by LPS, which suggested that QWZK inhibited TLR4/NF-κB signaling pathway and NLRP3 inflammasomes.Conclusions: The chemical compositions of QWZK were first identified. It was demonstrated that QWZK showed protective effects on ALI induced by LPS. The possible underlying mechanisms of QWZK on ALI induced by LPS was via inhibiting TLR4/NF-kB signaling pathway and NLRP3 inflammasome activation. This work suggested that QWZK is a potential therapeutic candidate for the treatments of ALI and pulmonary inflammation.

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Section: Discussionsupporting

confidence: 59%

Qingwenzhike Prescription Alleviates Acute Lung Injury Induced by LPS via Inhibiting TLR4/NF-kB Pathway and NLRP3 Inflammasome Activation

Zhang

Wang

et al. 2021

Front. Pharmacol.

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“…Previous studies have confirmed that NF-κB is also related to cellular apoptosis. However, some researchers have found that LPS could induce the activation of NF-κB, but NF-κB had no significant effect on LPSinduced apoptosis (Zhang, Lang, et al, 2020;Zhu et al, 2020).…”

Section: Results Of the Apoptosis Experimentsmentioning

confidence: 99%

“…According to reports, LPS is an important exogenous mediator that can induce the body's inflammatory response and is often used to establish inflammation models. Anthocyanins have been confirmed to inhibit the expression of cytokines in vitro and in vivo (Jiang et al., 2020 ; Qiu et al., 2021 ; Zhang, Lang, et al., 2020 ; Zhang, Xu, Zhao, et al., 2020 ). In this study, we found that C3G and C3G liposomes ameliorated LPS‐induced proinflammatory cytokines expression.…”

Section: Resultsmentioning

confidence: 99%

“…Haihua Zhang found that Echinacea polysaccharide may reduce inflammation and cellular apoptosis by inhibiting the TLR4/NF‐κB signaling pathway, thereby slowing down LPS‐induced lung injury. However, some researchers have found that LPS could induce the activation of NF‐κB, but NF‐κB had no significant effect on LPS‐induced apoptosis (Zhang, Lang, et al., 2020 ; Zhu et al., 2020 ). Evidence shows that anthocyanin‐rich riceberry bran extract could prevent apoptotic liver damage partly by attenuating oxidative stress and suppressing the activation of the NF‐κB pathway (Arjinajarn et al., 2017 ).…”

Section: Resultsmentioning

confidence: 99%

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Anti‐inflammatory activity of cyanidin‐3‐O‐glucoside and cyanidin‐3‐O‐glucoside liposomes in THP‐1 macrophages

Hao

Guan

Huang

et al. 2021

Food Science & Nutrition

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Inflammation is a response of the body to stimulation, which may be beneficial or harmful. Inflammation may either be acute or chronic, and is related to the homeostasis of physiological systems in vivo. Inflammation is associated with many diseases and is the basis of most pathological processes. The main causes of inflammation are infection and tissue damage, which can lead to the concentration of leukocytes and plasma proteins (Medzhitov, 2008).Chronic inflammation is involved in many diseases, including diabetes, obesity, atherosclerosis, and cancer (Coussens & Werb, 2002;

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“…Echinacea angustifolia is known to exhibit strong antimicrobial, anti-inflammatory, and anti-oxidant properties, as well as immune-modulating activity [ 219 , 220 ]. These effects have previously been demonstrated to be partly exerted by modulation of major inflammatory pathways, including NF-κB and MAPK [ 220 , 221 ]. The study which compared the effects of Echinacea angustifolia containing dietary supplementation to ESWT treatment of carpal tunnel patients showed that both strategies revealed improvements in pain and functionality in a comparable manner, indicating the potential of nutraceuticals to be embedded in future treatment strategies, since they represent a comfortable method for the management of carpal tunnel syndrome and other tendinopathies [ 216 ].…”

Section: Anti-inflammatory Effect Of Nutraceuticals On Tendinitis In ...mentioning

confidence: 99%

Modulation of Inflammation by Plant-Derived Nutraceuticals in Tendinitis

et al. 2022

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Tendinitis (tendinopathy) is a pro-inflammatory and painful tendon disease commonly linked with mechanical overuse and associated injuries, drug abuse, and lifestyle factors (including poor diet and physical inactivity) that causes significant healthcare expenditures due to its high incidence. Nuclear factor kappa B (NF-κB) is one of the major pro-inflammatory transcription factors, along with other inflammation signaling pathways, triggered by a variety of stimuli, including cytokines, endotoxins, physical and chemical stressors, hypoxia, and other pro-inflammatory factors. Their activation is known to regulate the expression of a multitude of genes involved in inflammation, degradation, and cell death. The pathogenesis of tendinitis is still poorly understood, whereas efficient and sustainable treatment is missing. Targeting drug suppression of the key inflammatory regulators represents an effective strategy for tendinitis therapy, but requires a comprehensive understanding of their principles of action. Conventional monotherapies are often ineffective and associated with severe side effects in patients. Therefore, agents that modulate multiple cellular targets represent therapeutic treatment potential. Plant-derived nutraceuticals have been shown to act as multi-targeting agents against tendinitis via various anti-oxidant and anti-inflammatory mechanisms, whereat they were able to specifically modulate numerous signaling pathways, including NF-κB, p38/MAPK, JNK/STAT3, and PI3K/Akt, thus down-regulating inflammatory processes. This review discusses the utility of herbal nutraceuticals that have demonstrated safety and tolerability as anti-inflammatory agents for the prevention and treatment of tendinitis through the suppression of catabolic signaling pathways. Limitations associated with the use of nutraceuticals are also described.

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Echinacea polysaccharide alleviates LPS-induced lung injury via inhibiting inflammation, apoptosis and activation of the TLR4/NF-κB signal pathway

Cited by 47 publications

References 48 publications

Qingwenzhike Prescription Alleviates Acute Lung Injury Induced by LPS via Inhibiting TLR4/NF-kB Pathway and NLRP3 Inflammasome Activation

Qingwenzhike Prescription Alleviates Acute Lung Injury Induced by LPS via Inhibiting TLR4/NF-kB Pathway and NLRP3 Inflammasome Activation

Anti‐inflammatory activity of cyanidin‐3‐O‐glucoside and cyanidin‐3‐O‐glucoside liposomes in THP‐1 macrophages

Modulation of Inflammation by Plant-Derived Nutraceuticals in Tendinitis

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