Cordycepin inhibits LPS-induced acute lung injury by inhibiting inflammation and oxidative stress

Lei, Jiaji; Wei, Youlei; Song, Peng; Li, Yongchao; Zhang, Tianze; Feng, Qian; Xu, Guohai

doi:10.1016/j.ejphar.2017.10.029

Cited by 152 publications

(104 citation statements)

References 26 publications

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“…Since free radicals may further promote the release of inflammatory cytokines (37), the present study also revealed that a significant increase in the release of inflammatory cytokines il-1β (P<0.05 in the lung and P<0.01 in the plasma) and TnF-α (P<0.05 in the lung and P<0.01 in the plasma) in the lung during iir was also inhibited by deX. among the oxidation products, Mda (38) and Sod (39) are always used to assess the degree of oxidative stress. The affinity of DEX binding to α2-adrenergic receptors is 8-fold greater compared with that of clonidine, and deX has a half-life of 6 min and an elimination half-life of 2 h (29,40).…”

Section: Discussionsupporting

confidence: 63%

Pretreatment with dexmedetomidine alleviates lung injury in a rat model of intestinal ischemia reperfusion

Chen

Bian

2020

Mol Med Report

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The aim of the present study was to investigate the antioxidant mechanisms of dexmedetomidine against lung injury during intestinal ischemia reperfusion (iir) in rats. The model of iir-induced acute lung injury was established by occluding the superior mesenteric artery (SMa) for 1 h and reperfusing for 2 h using Sprague-dawley rats. Pathological examination was used to assess the extent of the lung injury. oxidative stress was evaluated by measuring malondialdehyde, myeloperoxidase and superoxide dismutase in the lung and plasma. The proinflammatory cytokines tumor necrosis factor-α and interleukin-6 were determined via an enzyme-linked immunosorbent assay. The mrna and protein expression of nuclear factor-erythroid 2 related factor 2 (nrf2) and heme oxygenase 1 (Ho-1) were determined using a reverse transcription-quantitative polymerase chain reaction and western blotting. Pretreatment with dexmedetomidine significantly inhibited the oxidative stress response and proinflammatory factor release caused by IIR compared with the normal saline group (Mda and Sod in lung and plasma, P<0.05; MPo, il-1β and TnF-α in lung and plasma, P<0.05). dexmedetomidine improved pulmonary pathological changes in iir rats compared with the normal saline group. investigations into the molecular mechanism revealed that dexmedetomidine increased the expression levels of nrf2 and Ho-1 via activating α2 adrenergic receptors compared with the normal saline group. The antagonism of α2 adrenergic receptors may reverse the protective effect of dexmedetomidine on lung injury during iir, including decreasing the expression levels of nrf2 and Ho-1, elevating the oxidative stress response and increasing the proinflammatory factor release. in conclusion, pretreatment with dexmedetomidine demonstrated protective effects against lung injury during iir via α2 adrenergic receptors. The nrf2/Ho-1 signaling pathway may serve a function in the protective effect of dexmedetomidine.

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Section: Discussionsupporting

confidence: 63%

Pretreatment with dexmedetomidine alleviates lung injury in a rat model of intestinal ischemia reperfusion

Chen

Bian

2020

Mol Med Report

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“…Among these mechanisms, the accumulation of intermediates of oxidative stress has received great attention. 41,42 43 In the present study, the antioxidant capacity of LS174T was inhibited in the LPS group, mainly due to a significant decrease in SOD, GPx, CAT, and T-AOC enzyme activities. At present, the exact mechanism underlying the effects of ICA and pICA is not fully understood, but it may be related to the antioxidant properties of ICA and pICA.…”

Section: Discussionmentioning

confidence: 46%

The protective effect of icariin and phosphorylated icariin against LPS-induced intestinal goblet cell dysfunction

Xiong

Zhu

et al. 2019

Innate Immun

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In this study, we used LS174T cells as a model to investigate the protective effects of icariin and phosphorylated icariin on LPS-induced goblet cell dysfunction. Our results indicated that icariin and phosphorylated icariin increased the cell viability and decreased lactate dehydrogenase activity in LPS-treated LS174T cells. Icariin and phosphorylated icariin attenuated LPS-induced changes in mucin 2 synthesis and secretion. Besides, Icariin and phosphorylated icariin reduced the levels of ROS, MDA, and H2O2 and increased the activity of SOD, GPx, CAT, and T-AOC in LPS-treated LS174T cells. Moreover, the levels of IL-1β, IL-6, IL-8, and TNF-α were reduced in the Icariin and phosphorylated icariin group. Furthermore, Icariin and phosphorylated icariin decreased gene abundance or enzyme activity of Bip, XBP1, GRP78, CHOP, caspase-3, and caspase-4 in LPS-treated LS174T cells. Our data suggest that Icariin and phosphorylated icariin effectively attenuate LPS-induced intestinal goblet cell function damage through regulating oxidative stress, inflammation, apoptosis, and mucin expression.

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“…LPS is the main component of gram-negative bacteria. It is reported that LPS can activate cytokines through a series of cell signal transduction, which promote the release of a large number of inflammatory factors, subsequently induce cell apoptosis, and lead to the occurrence of ALI [17][18][19][20]. In this study, in vitro experiments investigated the effects of different doses of LPS (100 ng/mL, 500 ng/mL, and 1 μg/mL) on human pulmonary artery endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of MCP-1 in Acute Lung Injury and Advanced Therapy by Drug-Loaded Dextrin Nanoparticle

Cao

Liu

et al. 2018

International Journal of Polymer Science

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Objective. To observe the expression of monocyte chemotactic protein 1 (MCP-1) in acute lung injury (ALI) rat model, to characterize its effect on the development and progression of ALI, and to identify the potential new drug delivery approach during in vivo experiment. Method. The effects of different doses of lipopolysaccharide (LPS) on human pulmonary artery endothelial cells (HPAEC) were tested. For the animal experiments, thirty Sprague-Dawley (SD) rats were divided into physiological saline control group (NC group), the LPS model group (L group), the antagonist RS102895 combined with LPS group (R + L group), and the antagonist RS102895-loaded polyaldehyde dextran nanoparticles combined with LPS group (DNPR + L group). The blood gas analysis and dry/wet weight ratio were detected 24 hours after interventions. The levels of inflammatory factors, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), were tested by ELISA. The expression of monocyte chemoattractant protein-1 (MCP-1) in lung tissues was examined through Western blot, and the change of MCP-1 mRNA expression level was detected by performing RT-PCR. Result. LPS was responsible for inducing ALI in rats, and the degree of cell damage was dose-dependent. Blood gas analysis of L group showed that PaO2 and PaO2/FiO2 levels were significantly lower than those of the NC group (P<0.05), while the dry/wet weight ratio of lung tissues in L group increased (P<0.05). Inflammatory factors including TNF-α and IL-1β and the expression of MCP-1 in both protein and mRNA levels were higher in L group than in the NC group (P<0.05). The inhibition of the interaction between MCP-1 and chemokines receptor 2 (CCR2) by antagonist RS102895 can significantly alleviate the ALI in rats, which is accompanied by a significant decrease of inflammatory factors and MCP-1 expression (P<0.05). Compared with R + L group, treatment with DNPR and LPS combination significantly improved the condition of rats and decreased the level of TNF-α, IL-1β, and MCP-1 expression (P<0.05). Conclusion. In ALI, RS102895 can inhibit the MCP-1/CCR2 interaction, therefore, retarding the progress of ALI. Because of the high transfection efficiency of inhibitor RS102895packgaed by polyaldehyde dextran nanoparticles, this phenomenon particularly reached a significant level. The results imply new insights for the treatment of ALI.

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Cordycepin inhibits LPS-induced acute lung injury by inhibiting inflammation and oxidative stress

Cited by 152 publications

References 26 publications

Pretreatment with dexmedetomidine alleviates lung injury in a rat model of intestinal ischemia reperfusion

Pretreatment with dexmedetomidine alleviates lung injury in a rat model of intestinal ischemia reperfusion

The protective effect of icariin and phosphorylated icariin against LPS-induced intestinal goblet cell dysfunction

Mechanism of MCP-1 in Acute Lung Injury and Advanced Therapy by Drug-Loaded Dextrin Nanoparticle

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