Icariside II attenuates lipopolysaccharide-induced neuroinflammation through inhibiting TLR4/MyD88/NF-κB pathway in rats

Zhou, Jiayin; Deng, Yuanyuan; Li, Fēi; Yin, Caixia; Shi, Jingshan; Gong, Qihai

doi:10.1016/j.biopha.2018.10.201

Cited by 90 publications

(42 citation statements)

References 36 publications

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“…Inactivation of NF-κB was found to result directly in a decreased pro-inflammatory mediator production including TNF-α, IL-6, IL-12 and IL-1β, all indicators of a severe inflammatory response [46]. Importantly, NF-κB is the key target of p38 MAPK and Akt signaling pathways after LPS binding TLR4/MYD88 to initiate intracellular pathways [11,12]. Both p38 MAPK/MK2 and PI3K-Akt can regulate LPS-induced gene expression by controlling NF-kB p65 hyperphosphorylation and nuclear translocation [47,48,49].…”

Section: Discussionmentioning

confidence: 99%

“…Exposure to LPS causes inflammatory cell infiltration, leading to generation of cytokines and chemokines that subsequently lead to initiation and propagation of the inflammation response seen in ALI/ARDS [10]. LPS binds Toll-like receptor 4 (TLR4) on the cell surface which then stimulates the recruitment and activation of the adaptor protein myeloid differentiation primary response gene 88 (MYD88) to the receptor complex, in turn leading to the activation of intracellular pathways [11,12]. p38 MAPK has been demonstrated to be an important kinase activated by TLR4/MyD88, phosphorylation of its downstream kinases, MK2, enhances mRNA levels and stability of cytokines such as TNF-α, IL-6 and IL-12 [13,14].…”

Section: Introductionmentioning

confidence: 99%

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Dehydrocostus Lactone Suppresses LPS-induced Acute Lung Injury and Macrophage Activation through NF-κB Signaling Pathway Mediated by p38 MAPK and Akt

et al. 2019

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Acute lung injury (ALI) is a severe clinical disease marked by dysregulated inflammation response and has a high rate of morbidity and mortality. Macrophages, which play diverse roles in the inflammatory response, are becoming therapeutic targets in ALI. In this study we investigated the effects of dehydrocostus lactone (DHL), a natural sesquiterpene, on macrophage activation and LPS-induced ALI. The macrophage cell line RAW264.7 and primary lung macrophages were incubated with DHL (0, 3, 5, 10 and 30 μmol/L) for 0.5 h and then challenged with LPS (100 ng/mL) for up to 8 hours. C57BL/6 mice were intratracheally injected with LPS (5 mg/kg) to induce acute lung injury (ALI) and then treated with a range of DHL doses intraperitoneally (5 to 20 mg/kg). The results showed that DHL inhibited LPS-induced production of proinflammatory mediators such as iNOS, NO, and cytokines including TNF-α, IL-6, IL-1β, and IL-12 p35 by suppressing the activity of NF-κB via p38 MAPK/MK2 and Akt signaling pathway in macrophages. The in vivo results revealed that DHL significantly attenuated LPS-induced pathological injury and reduced cytokines expression in the lung. NF-κB, p38 MAPK/MK2 and Akt signaling molecules were also involved in the anti-inflammatory effect. Collectively, our findings suggested that DHL is a promising agent for alleviating LPS-induced ALI.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Dehydrocostus Lactone Suppresses LPS-induced Acute Lung Injury and Macrophage Activation through NF-κB Signaling Pathway Mediated by p38 MAPK and Akt

et al. 2019

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“…cytokines such as TNF-α, IL-6, IL-1β and iNOS [52]. Hence, protein modeling for TNF-α, IL-6, IL-1β and iNOS using three servers; I-TASSER, RaptorX, and SWISS-MODEL was performed.…”

Section: Plos Onementioning

confidence: 99%

Betanin purification from red beetroots and evaluation of its anti-oxidant and anti-inflammatory activity on LPS-activated microglial cells

et al. 2020

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Microglial activation can release free radicals and various pro-inflammatory cytokines, which implicates the progress of a neurodegenerative disease. Therefore suppression of microglial activation can be an appropriate strategy for combating neurodegenerative diseases. Betanin is a red food dye that acts as free radical scavenger and can be a promising candidate for this purpose. In this study, purification of betanin from red beetroots was carried out by normal phase colum chromatography, yielding 500 mg of betanin from 100 g of red beetroot. The purified betanin was evaluated by TLC, UV-visible, HPLC, ESI-MASS, FT-IR spectroscopy. Investigation on the inhibitory effect of betanin on activated microglia was performed using primary microglial culture. The results showed that betanin significantly inhibited lipopolysaccharide induced microglial function including the production of nitric oxide free radicals, reactive oxygen species, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and interleukin-1 beta (IL-1β). Moreover, betanin modulated mitochondrial membrane potential, lysosomal membrane permeabilization and adenosine triphosphate. We further investigated the interaction of betanin with TNF-α, IL-6 and Nitric oxide synthase (iNOS or NOS2) using in silico molecular docking analysis. The docking results demonstrated that betanin have significant negative binding energy against active sites of TNF-α, IL-6 and iNOS.

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“…To date, many researchers have studied TLR1 to TLR10, and TLR4 was the primary receptor for LPS, thereby conferring the recognition of gram-negative bacteria [3,4,5,6,7,8]. LPS-induced TLR4 signaling pathways showed that TLR4, CD14 and Myd88 complexes were the indispensable components to recognize LPS [9,10,11,12]. Additionally, it has demonstrated that LPS treatment not only affected immune cells such as T cells and macrophage, but also had an impact on many types of epithelial cells through TLR4 signaling, which led to local infections or inflammatory processes [13].…”

Section: Introductionmentioning

confidence: 99%

L-Arginine Inhibited Inflammatory Response and Oxidative Stress Induced by Lipopolysaccharide via Arginase-1 Signaling in IPEC-J2 Cells

Qiu

Yang

Wang

et al. 2019

IJMS

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This study aimed to explore the effect of L-arginine on lipopolysaccharide (LPS)-induced inflammatory response and oxidative stress in IPEC-2 cells. We found that the expression of toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), cluster of differentiation 14 (CD14), nuclear factor-kappaBp65 (NF-κBp65), chemokine-8 (IL-8), tumor necrosis factor (TNF-α) and chemokine-6 (IL-6) mRNA were significantly increased by LPS. Exposure to LPS induced oxidative stress as reactive oxygen species (ROS) and malonaldehyde (MDA) production were increased while glutathione peroxidase (GSH-Px) were decreased in LPS-treated cells compared to those in the control. LPS administration also effectively induced cell growth inhibition through induction of G0/G1 cell cycle arrest. However, compared with the LPS group, cells co-treatment with L-arginine effectively increased cell viability and promoted the cell cycle into the S phase; L-arginine exhibited an anti-inflammatory effect in alleviating inflammation induced by LPS by reducing the abundance of TLR4, MyD88, CD14, NF-κBp65, and IL-8 transcripts. Cells treated with LPS+L-arginine significantly enhanced the content of GSH-Px, while they decreased the production of ROS and MDA compared with the LPS group. Furthermore, L-arginine increased the activity of arginase-1 (Arg-1), while Arg-1 inhibitor abolished the protection of arginine against LPS-induced inflammation and oxidative stress. Taken together, these results suggested that L-arginine exerted its anti-inflammatory and antioxidant effects to protect IPEC-J2 cells from inflammatory response and oxidative stress challenged by LPS at least partly via the Arg-1 signaling pathway.

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Icariside II attenuates lipopolysaccharide-induced neuroinflammation through inhibiting TLR4/MyD88/NF-κB pathway in rats

Cited by 90 publications

References 36 publications

Dehydrocostus Lactone Suppresses LPS-induced Acute Lung Injury and Macrophage Activation through NF-κB Signaling Pathway Mediated by p38 MAPK and Akt

Dehydrocostus Lactone Suppresses LPS-induced Acute Lung Injury and Macrophage Activation through NF-κB Signaling Pathway Mediated by p38 MAPK and Akt

Betanin purification from red beetroots and evaluation of its anti-oxidant and anti-inflammatory activity on LPS-activated microglial cells

L-Arginine Inhibited Inflammatory Response and Oxidative Stress Induced by Lipopolysaccharide via Arginase-1 Signaling in IPEC-J2 Cells

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