2020
DOI: 10.1016/j.freeradbiomed.2019.11.011
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Galectin-1 ameliorates lipopolysaccharide-induced acute lung injury via AMPK-Nrf2 pathway in mice

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Cited by 89 publications
(116 citation statements)
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“…Thus, our findings indicate that SP has potent antioxidant properties that are likely to be responsible for its protective effect against acute lung damage that is caused by LPS treatment. Nrf2 plays an essential role in many inflammatory-and oxidative stress-related diseases, such as chronic obstructive pulmonary disease (COPD) and ALI [14,18]. Nrf2 protects a variety of tissue and cells against ROS through ARE-mediated induction of diverse antioxidant enzymes, including HO-1 and NQO1 [54].…”
Section: Discussionmentioning
confidence: 99%
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“…Thus, our findings indicate that SP has potent antioxidant properties that are likely to be responsible for its protective effect against acute lung damage that is caused by LPS treatment. Nrf2 plays an essential role in many inflammatory-and oxidative stress-related diseases, such as chronic obstructive pulmonary disease (COPD) and ALI [14,18]. Nrf2 protects a variety of tissue and cells against ROS through ARE-mediated induction of diverse antioxidant enzymes, including HO-1 and NQO1 [54].…”
Section: Discussionmentioning
confidence: 99%
“…The activation of NF-κB and MAPK pathways collaborates to induce the release of various pro-inflammatory cytokines or chemokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 [12,13]. Oxidative stress also plays a major role in the pathogenesis of lung injury in LPS-induced ALI [14,15]. Nuclear factor erythroid-2 related factor 2 (Nrf2) is a redox-sensitive transcription factor and it regulates the antioxidant and detoxifying enzymes [16].…”
Section: Introductionmentioning
confidence: 99%
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“…These findings were consistent with the reduced RANTES, IL-6 and IL-1β we found and strongly support our results. Currently, there is increasing evidence suggesting that the infiltration of macrophages (Johnston et al, 2012;Huang et al, 2020) and neutrophils (Camp and Jonsson, 2017) are key factors in the pathogenesis of IAV-induced ALI and ARDS, especially at the early stage of disease (Huang et al, 2018), and is accompanied by an increase in the immune-pathological injury of IAV infection (Camp and Jonsson, 2017;Huang et al, 2020). Thus, the reduction of inflammatory cytokines, chemokines and cell numbers after Gal-1 treatment might have a positive effect on H1N1pdm09-induced ALI.…”
Section: Discussionmentioning
confidence: 99%
“…Taken together, these results provide a potential strategy for the regulation of CYP1A1 expression in ALI. Excessive pro-inflammatory mediator production is a significant cause of ALI tissue damage [21][22][23][24]. Thus, the aim of this study was to identify a novel target for treatment of ALI, a target that would reduce a pro-inflammatory response.…”
Section: Discussionmentioning
confidence: 99%