Curcumin attenuates IL-17A mediated pulmonary SMAD dependent and non-dependent mechanism during acute lung injury in vivo

Shaikh, Sadiya Bi; Bhat, Sinchana G; Bhandary, Yashodhar P.

doi:10.1007/s11033-020-05587-0

Cited by 12 publications

(8 citation statements)

References 21 publications

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“…IL-17A is an early promoter of T-cell-induced inflammatory response, which can be amplified by promoting the release of pre-inflammatory cytokines (16). IL-17A serves a crucial role in the inflammatory reaction, tissue damage and immunological defense (17)(18)(19). A previous study revealed that IL-17A may be involved in H9c2 cell development (20).…”

Section: Introductionmentioning

confidence: 99%

miR‑126‑5p regulates H9c2 cell proliferation and apoptosis under hypoxic conditions by targeting IL‑17A

et al. 2020

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Accumulating evidence has indicated that microRNAs (miRNAs/miRs) regulate the occurrence and development of various diseases, including diabetes, osteoporosis and cardiovascular conditions. However, the role of miRNAs in acute myocardial infarction (AMI) is not completely understood. The present study aimed to evaluate the therapeutic efficacy and mechanisms underlying the effects of miR-126-5p on H9c2 cell proliferation and apoptosis by targeting interleukin (IL)-17A. A total of 40 patients with AMI and 40 healthy volunteers were recruited in the present study and the expression levels of serum miR-126-5p and IL-17A were determined. Following confirmation that IL-17A was a target of miR-126-5p via a dual-luciferase reporter assay, H9c2 cells were exposed to hypoxic conditions. H9c2 cell viability and apoptosis were subsequently assessed. Additionally, the protein expression levels of apoptosis-associated proteins were detected following transfection. Compared with healthy individuals, miR-126-5p expression was significantly decreased in the serum samples of patients with AMI, whereas IL-17A, the target of miR-126-5p, was significantly increased. Following hypoxic treatment, miR-126-5p overexpression enhanced H9c2 cell viability compared with the NC group, which was subsequently reversed following co-transfection with pcDNA3.1-IL-17A. Additionally, the results indicated that hypoxia-induced H9c2 cell apoptosis was significantly reduced following transfection with miR-126-5p mimics via the PI3K/AKT signaling pathway compared with the NC group. The present study indicated that miR-126-5p may serve as a novel miRNA that regulates H9c2 cell viability and apoptosis by targeting IL-17A under hypoxic conditions. Therefore, miR-126-5p may serve as a crucial biomarker for the diagnosis of AMI.

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Section: Introductionmentioning

confidence: 99%

miR‑126‑5p regulates H9c2 cell proliferation and apoptosis under hypoxic conditions by targeting IL‑17A

et al. 2020

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“…In the mouse model of severe influenza A pneumonia, IL-6 promoted muscle degradation via the E3 Ubiquitin Ligase atrogin-1, STAT3, FOXO3a (Shaikh, Bhat & Bhandary, 2020). There is also study shows that glucocorticoids potentiate IL-6-induced SP-B expression in H441 cells by enhancing the JAK-STAT signaling pathway and that phenomenon is reversed by JAK1 inhibitor (Ladenburger et al, 2010b).…”

Section: Jak/stat Expression Pattern In Lungmentioning

confidence: 99%

“…JAK1-associated PI3K signaling regulates gene induction of inflammation cytokines 53 . In addition, IL-17A is revealed of participating in the acute lung injury process, it upregulated p-JAK1/2, p-STAT1/3, stimulated inflammation gene induction in human airway epithelial cells by JAK1-associated PI3K signaling (Shaikh, Bhat & Bhandary, 2020). In the respiratory inflammatory response process, JAK1 and STAT3 stimulated the -500 to +41 promoter activity of the surfactant protein B (SP-B) gene in respiratory epithelial cells, influence on surfactant protein homeostasis (Yan, Naltner, Martin, Naltner, Fangman & Gurel, 2002).…”

Section: Jak/stat Expression Pattern In Lungmentioning

confidence: 99%

“…There is also study shows that glucocorticoids potentiate IL-6-induced SP-B expression in H441 cells by enhancing the JAK-STAT signaling pathway and that phenomenon is reversed by JAK1 inhibitor (Ladenburger et al, 2010b). Not only IL-6, there are many other cytokines, like IL-17A participated in the in vivo mice model of ALI, may related to ARDS (Shaikh, Bhat & Bhandary, 2020).…”

Section: Jak/stat Expression Pattern In Lungmentioning

confidence: 99%

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JAK-STAT signaling as an ARDS therapeutic target: status and future trends

Zhang

Gao

Yan

et al. 2022

Preprint

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Acute respiratory distress syndrome (ARDS) is an acute respiratory disease which is characterized by non-cardiogenic pulmonary oedema. It has a high mortality rate and lacks effective pharmacotherapy. As the outbreak of COVID worldwide, the mortality of ARDS has increased correspondingly, which makes it urgent to find effective targets and strategies for the treatment of ARDS. Recent clinical trials of Janus kinase (JAK) inhibitors in treating COVID induced ARDS have shown a positive outcome, which makes the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway a potential therapeutic target for treating ARDS. Here, we review the complex cause of ARDS, the molecular pathway of JAK/STAT involved in ARDS pathology, and the progress that has been made in strategies of targeting JAK/STAT to treat ARDS Specially, JAK/STAT signaling directly participates in the progression of ARDS or collude with other pathways to aggravate ARDS. We summarize JAK and STAT inhibitors with ARDS treatment benefits, including inhibitors in clinical trials and pre-clinical studies and natural products, and discuss the side effects of the current JAK inhibitors to reveal the future trends in designing of JAK inhibitors, which will help to develop effective treatment strategies for ARDS in the future.

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“…A previous study showed that curcumin might inhibit the activation of NLRP3 inflammasome-dependent pyrolysis by upregulating SIRT1, which in so doing inhibits inflammation [ 84 ]. Moreover, a large number of studies showed that curcumin has a significant inhibitory effect on IL-17A-mediated downstream pathways, including MCM2, MCM3, MCM6 [ 85 ], SMAD-dependent pathway (SMAD2/SMAD3 ) and non-SMAD-dependent ( JAK1/JAK2, STAT-1/STAT-3 ) pathway [ 86 ], p53/PAI-1 signaling pathway [ 87 ]. Interestingly, to improve the anti-inflammatory effect of curcumin, it is often loaded on a carrier and delivered to the lungs.…”

Section: The Application Of Antioxidants In Alimentioning

confidence: 99%

Friend or Foe? The Roles of Antioxidants in Acute Lung Injury

Yang

Zhou

et al. 2021

Antioxidants

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Acute lung injury (ALI) is an acute hypoxic respiratory insufficiency caused by various intra- and extra-pulmonary injury factors. The oxidative stress caused by excessive reactive oxygen species (ROS) produced in the lungs plays an important role in the pathogenesis of ALI. ROS is a “double-edged sword”, which is widely involved in signal transduction and the life process of cells at a physiological concentration. However, excessive ROS can cause mitochondrial oxidative stress, leading to the occurrence of various diseases. It is well-known that antioxidants can alleviate ALI by scavenging ROS. Nevertheless, more and more studies found that antioxidants have no significant effect on severe organ injury, and may even aggravate organ injury and reduce the survival rate of patients. Our study introduces the application of antioxidants in ALI, and explore the mechanisms of antioxidants failure in various diseases including it.

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Curcumin attenuates IL-17A mediated pulmonary SMAD dependent and non-dependent mechanism during acute lung injury in vivo

Cited by 12 publications

References 21 publications

miR‑126‑5p regulates H9c2 cell proliferation and apoptosis under hypoxic conditions by targeting IL‑17A

miR‑126‑5p regulates H9c2 cell proliferation and apoptosis under hypoxic conditions by targeting IL‑17A

JAK-STAT signaling as an ARDS therapeutic target: status and future trends

Friend or Foe? The Roles of Antioxidants in Acute Lung Injury

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