Glucosamine attenuates cigarette smoke-induced lung inflammation by inhibiting ROS-sensitive inflammatory signaling

Wu, Yuh Lin; Lin, An Hsuan; Chen, Chao Hung; Huang, Wen Chien; Wang, Hsin‐Yi; Liu, Meng Han; Lee, Tzong‐Shyuan; Kou, Yu Ru

doi:10.1016/j.freeradbiomed.2014.01.026

Cited by 50 publications

(85 citation statements)

References 57 publications

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“…ROS are an important trigger for the induction of IL-8 by CSE in HBECs [4, 7, 8]. Relative to control cells, exposure of HBECs to 3% CSE for 2 and 30 minutes resulted in increases in both the extracellular (Figure 6(a)) and intracellular levels (Figure 6(b)) of ROS, respectively.…”

Section: Resultsmentioning

confidence: 99%

“…The murine model of chronic CS exposure has been described in detail previously [7, 8, 27]. Briefly, male C57BL/6J mice at the age of 8 weeks (National Laboratory Animal Center, Taipei, Taiwan) were randomly divided into four groups ( n = 7 mice/group) for exposure to air or CS.…”

Section: Methodsmentioning

confidence: 99%

“…CSE was freshly prepared on the day of the experiment as previously described [7, 8] with some modifications. In brief, 1000 mL of the smoke generated from two burning cigarettes (Marlboro Red Label, Philip Morris, Richmond, VA, USA) without filters was sucked under a constant flow rate (8 mL/s) into a syringe and then bubbled into a tube containing 20 mL serum-free medium.…”

Section: Methodsmentioning

confidence: 99%

“…The induction of inflammatory mediators by CS in lung cells is mainly regulated by redox-sensitive signaling pathways [4, 6–9]. Initially, CS may increase the intracellular levels of reactive oxygen species (ROS) in lung epithelial cells [4, 7, 8] or other types of lung cells [9–12]. Subsequently, this increased intracellular ROS may activate various ROS-sensitive signaling pathways, such as the mitogen-activated protein kinases (MAPKs) and a number of downstream transcriptional factors, such as nuclear factor- κ B (NF- κ B), and ultimately promote inflammatory gene expression [4, 6–12].…”

Section: Introductionmentioning

confidence: 99%

“…We employed an established murine model of chronic CS exposure [7, 8, 27] to assess the inhibitory effects of paeonol on oxidative stress and various indices of lung inflammation. Additionally, we used an established in vitro model of primary human bronchial epithelial cells (HBECs) [7, 8] to determine the suppressive effects of paeonol on increases in intracellular ROS, activation of the ROS-sensitive inflammatory signaling pathways, and the induction of interleukin-8 (IL-8), all of which are mediated by CS extract (CSE).…”

Section: Introductionmentioning

confidence: 99%

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Paeonol Attenuates Cigarette Smoke-Induced Lung Inflammation by Inhibiting ROS-Sensitive Inflammatory Signaling

Liu

Lin

Lee

et al. 2014

Mediators of Inflammation

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Cigarette smoking causes persistent lung inflammation that is mainly regulated by redox-sensitive pathways. We have previously reported that cigarette smoke (CS) activates reactive oxygen species- (ROS-) sensitive mitogen-activated protein kinases (MAPKs)/nuclear factor-κB (NF-κB) signaling leading to induction of lung inflammation. Paeonol, the main phenolic compound present in the Chinese herb Paeonia suffruticosa, has antioxidant and anti-inflammatory properties. However, whether paeonol has similar beneficial effects against CS-induced lung inflammation remains unclear. Using a murine model, we showed that chronic CS exposure for 4 weeks caused pulmonary inflammatory infiltration, increased lung vascular permeability, elevated lung levels of chemokines, cytokines, and 4-hydroxynonenal (an oxidative stress biomarker), and induced lung inflammation; all of these CS-induced events were suppressed by chronic treatment with paeonol. Using human bronchial epithelial cells (HBECs), we demonstrated that cigarette smoke extract (CSE) sequentially increased extracellular and intracellular levels of ROS, activated the MAPKs/NF-κB signaling, and induced interleukin-8 (IL-8); all these CSE-induced events were inhibited by paeonol pretreatment. Our findings suggest a novel role for paeonol in alleviating the oxidative stress and lung inflammation induced by chronic CS exposure in vivo and in suppressing CSE-induced IL-8 in vitro via its antioxidant function and an inhibition of the MAPKs/NF-κB signaling.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Paeonol Attenuates Cigarette Smoke-Induced Lung Inflammation by Inhibiting ROS-Sensitive Inflammatory Signaling

Liu

Lin

Lee

et al. 2014

Mediators of Inflammation

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Byproducts from Shellfish Harvesting and Processing

Klomklao

Poonsin

Benjakul

et al. 2019

Byproducts From Agriculture and Fisheries

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Structure Analysis and Anti‐Inflammatory Effect of a Polysaccharide from Hippocampus mohnikei

Cui

Wang

Liu

2022

Chemistry & Biodiversity

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The purpose of this study was to analyze the structure of a polysaccharide (HMP-1) from Hippocampus mohnikei, and to explore its anti-inflammatory effect. HMP-1 was obtained from Hippocampus mohnikei by ethanol sedimentation and secondary column chromatography purification. Its structural characteristics were analyzed by gel permeation chromatography (GPC), Fourier transform infrared (FT-IR) spectroscopy, nuclear magnetic resonance (NMR) spectroscopy and scanning electron micrograph (SEM). Results showed its molecular weight (Mw) was 7296 Da, and it mainly consisted of six residues: 1,3-β-Glcp, 1,4-α-Manp, 1,4-α-GalpA, 1,4-β-GlcpA2S, 1,4-α-Galp3S, and 1,4-β-GlcNAc. HMP-1 could protect RAW246.7 cells from the cytotoxic effect induced by LPS. HMP-1 also could reduce the levels of nitric oxide and reactive oxygen species produced by LPS stimulation, suggesting that HMP-1 has anti-inflammatory activities within a certain concentration range.

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Glucosamine attenuates cigarette smoke-induced lung inflammation by inhibiting ROS-sensitive inflammatory signaling

Cited by 50 publications

References 57 publications

Paeonol Attenuates Cigarette Smoke-Induced Lung Inflammation by Inhibiting ROS-Sensitive Inflammatory Signaling

Paeonol Attenuates Cigarette Smoke-Induced Lung Inflammation by Inhibiting ROS-Sensitive Inflammatory Signaling

Byproducts from Shellfish Harvesting and Processing

Structure Analysis and Anti‐Inflammatory Effect of a Polysaccharide from Hippocampus mohnikei

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