Resokaempferol-mediated anti-inflammatory effects on activated macrophages via the inhibition of JAK2/STAT3, NF-κB and JNK/p38 MAPK signaling pathways

Yu, Qian; Zeng, Ke‐Wu; Ma, Xiaoli; Song, Fang-Jiao; Jiang, Yong; Tu, Peng‐Fei; Wang, Xuemei

doi:10.1016/j.intimp.2016.05.010

Cited by 76 publications

(49 citation statements)

References 38 publications

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“…JAK/STAT3 signaling is an important oncogenic pathway that is involved in the carcinogenesis of many types of human cancers, including colorectal cancer, hepatocellular carcinoma and pancreatic cancer . Emerging studies have indicated that the JAK/STAT3 signaling plays an important role in the inflammatory response . Moreover, JAK/STAT3 signaling was reported to be implicated in the lung during the acute inflammatory injury, illuminating a potential target for anti‐inflammatory treatment .…”

Section: Discussionmentioning

confidence: 99%

Circ_0038467 regulates lipopolysaccharide‐induced inflammatory injury in human bronchial epithelial cells through sponging miR‐338‐3p

Liu

Wan

et al. 2020

Thoracic Cancer

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Background: Pneumonia is a common acute lower respiratory infection in children and elders. Circular RNAs (circRNAs) have recently been uncovered to play important roles in pneumonia. However, the function and mechanism of circ_0038467 in pneumonia remain elusive. Methods: Cell viability and apoptosis were determined using the Cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. The levels of interleukin 6 (IL-6), IL-8 and IL-1β were detected by enzyme-linked immunosorbent assay (ELISA). Western blot analysis was performed to assess the expression of related proteins. Circ_0038467 was characterized by Ribonuclease R (RNase) digestion and subcellular localization assays. The levels of circ_0038467 and miR-338-3p were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). The direct interaction between circ_0038467 and miR-338-3p was validated by the dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Results: Our data indicated that lipopolysaccharide (LPS) induced an inflammatory injury in 16HBE cells by repressing cell viability and enhancing cell apoptosis and proinflammatory cytokines production. Circ_0038467 was upregulated and miR-338-3p was downregulated in LPS-treated 16HBE cells. Circ_0038467 knockdown or miR-338-3p overexpression attenuated LPS-induced 16HBE cell inflammatory injury. Moreover, circ_0038467 acted as a sponge of miR-338-3p in 16HBE cells. MiR-338-3p mediated the alleviated effect of circ_0038467 knockdown on LPS-induced 16HBE cell inflammatory injury. Additionally, the Janus kinase/ signal transducer and activator of transcription 3 (JAK/STAT3) signaling pathway was involved in the circ_0038467/miR-338-3p axis-mediated regulation in LPS-induced 16HBE cell inflammatory injury. Conclusions: The current work had led to the identification of circ_0038467 knockdown that alleviated LPS-induced inflammatory injury in 16HBE cells at least partly through sponging miR-338-3p and regulating JAK/STAT3 pathway, highlighting novel molecular targets for the treatment of pneumonia.

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Section: Discussionmentioning

confidence: 99%

Circ_0038467 regulates lipopolysaccharide‐induced inflammatory injury in human bronchial epithelial cells through sponging miR‐338‐3p

Liu

Wan

et al. 2020

Thoracic Cancer

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“…Moreover, Yu et al testified that resokaempferol attenuates the activation of JNK and p38 but not ERK in LPS-induced inflammation RAW264.7 cells to achieve the anti-inflammatory effect (Yu et al, 2016). Lin et al also did not observe a significant alteration of ERK1/ 2 phosphorylation in human neuroblastoma SH-SY5Y cells treated by either glutamate or astaxanthin (Lin, Zhao, & Li, 2017).…”

Section: Discussionmentioning

confidence: 99%

β‐carotene attenuates lipopolysaccharide‐induced inflammation via inhibition of the NF‐κB, JAK2/STAT3 and JNK/p38 MAPK signaling pathways in macrophages

Pan

Zheng

2018

Animal Science Journal

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β-carotene is one of the most abundant carotenoids, has potential anti-inflammatory effect, it has been reported that β-carotene could suppress LPS-induced inflammatory responses by inhibiting nuclear factor kappa B (NF-κB) translocation, but the more detailed molecular mechanisms underlying the anti-inflammatory action of βcarotene remain to be fully understood. In this study, we investigated the influence of β-carotene on the activation of JAK2/STAT3, MAPK, and NF-κB signaling pathway induced by LPS in RAW264.7 cells and peritoneal macrophages. Cells were treated with different concentrations of β-carotene for 3 hr after LPS treatment for 24 hr. The mRNA expression and the release of IL-1β, IL-6, and TNF-α were evaluated by RT-PCR and ELISA, and the level of signaling proteins of JAK2/STAT3, MAPK, and NF-κB signaling pathway were detected by Western blot. The results showed that β-carotene significantly suppressed (p < 0.05) LPS-induced release of IL-1β, IL-6, and TNF-α and their mRNA expression. LPS-induced JAK2/STAT3, IκB/ NF-κB p65, JNK/p38 MAPK signal activation were significantly attenuated (p < 0.05) by β-carotene in a dose-dependent manner. In conclusion, β-carotene could attenuate LPS-induced inflammation via inhibition of the NF-κB, JAK2/STAT3, and JNK/p38 MAPK signaling pathways in macrophages.

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“…Therefore, STAT1 could contribute to iNOS upregulation in the diabetic lung [96,97]. The pro-inflammatory role of the JAK/STAT pathway is well established in the macrophage [98,99,100]. Antioxidants such as resveratrol have been reported to inhibit inflammatory pathways in mouse macrophages by inhibiting JAK/STAT signaling pathways, suggesting that DM-induced oxidative stress in the lung, contributing to DM-induced lung inflammation, could be mediated via JAK/STAT activation [98].…”

Section: Putative Signaling Mediating Diabetes-induced Microvasculmentioning

confidence: 99%

Diabetic Microvascular Disease and Pulmonary Fibrosis: The Contribution of Platelets and Systemic Inflammation

Jagadapillai

Rane

Lin

et al. 2016

IJMS

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Diabetes is strongly associated with systemic inflammation and oxidative stress, but its effect on pulmonary vascular disease and lung function has often been disregarded. Several studies identified restrictive lung disease and fibrotic changes in diabetic patients and in animal models of diabetes. While microvascular dysfunction is a well-known complication of diabetes, the mechanisms leading to diabetes-induced lung injury have largely been disregarded. We described the potential involvement of diabetes-induced platelet-endothelial interactions in perpetuating vascular inflammation and oxidative injury leading to fibrotic changes in the lung. Changes in nitric oxide synthase (NOS) activation and decreased NO bioavailability in the diabetic lung increase platelet activation and vascular injury and may account for platelet hyperreactivity reported in diabetic patients. Additionally, the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway has been reported to mediate pancreatic islet damage, and is implicated in the onset of diabetes, inflammation and vascular injury. Many growth factors and diabetes-induced agonists act via the JAK/STAT pathway. Other studies reported the contribution of the JAK/STAT pathway to the regulation of the pulmonary fibrotic process but the role of this pathway in the development of diabetic lung fibrosis has not been considered. These observations may open new therapeutic perspectives for modulating multiple pathways to mitigate diabetes onset or its pulmonary consequences.

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Resokaempferol-mediated anti-inflammatory effects on activated macrophages via the inhibition of JAK2/STAT3, NF-κB and JNK/p38 MAPK signaling pathways

Cited by 76 publications

References 38 publications

Circ_0038467 regulates lipopolysaccharide‐induced inflammatory injury in human bronchial epithelial cells through sponging miR‐338‐3p

Circ_0038467 regulates lipopolysaccharide‐induced inflammatory injury in human bronchial epithelial cells through sponging miR‐338‐3p

β‐carotene attenuates lipopolysaccharide‐induced inflammation via inhibition of the NF‐κB, JAK2/STAT3 and JNK/p38 MAPK signaling pathways in macrophages

Diabetic Microvascular Disease and Pulmonary Fibrosis: The Contribution of Platelets and Systemic Inflammation

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