Ellipticine blocks synergistic effects of IL-17A and TNF-α in epithelial cells and alleviates severe acute pancreatitis-associated acute lung injury

Li, Xingli; Ye, Chenxian; Mulati, Mubarak; Sun, Lei; Qian, Feng

doi:10.1016/j.bcp.2020.113992

Cited by 27 publications

(21 citation statements)

References 39 publications

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“…The combination of IL-17 and TNF-α inhibitors has shown better efficacy in inflammatory diseases. In SAP, ellipticine attenuated NF-κB and MAPK activation in response to IL-17A and TNF-α treatment, inhibited Act1- and TRAF6-mediated NF-κB activation, and blocked the interaction of Act1 with TRAF6 ( 133 ). The IL-6/STAT3 signaling pathway is a vital regulator of Th17 and Treg cells by promoting Th17 cells and inhibiting the differentiation of Tregs.…”

Section: Therapeutic Implications Of Apmentioning

confidence: 99%

Role of Interleukin-17 in Acute Pancreatitis

Chen

Liu

et al. 2021

Front. Immunol.

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Acute pancreatitis (AP) is a leading cause of death and is commonly accompanied by systemic manifestations that are generally associated with a poor prognosis. Many cytokines contribute to pancreatic tissue damage and cause systemic injury. Interleukin-17 (IL-17) is a cytokine that may play a vital role in AP. Specifically, IL-17 has important effects on the immune response and causes interactions between different inflammatory mediators in the AP-related microenvironment. In this literature review, we will discuss the existing academic understanding of IL-17 and the impacts of IL-17 in different cells (especially in acinar cells and immune system cells) in AP pathogenesis. The clinical significance and potential mechanisms of IL-17 on AP deterioration are emphasized. The evidence suggests that inhibiting the IL-17 cytokine family could alleviate the pathogenic process of AP, and we highlight therapeutic strategies that directly or indirectly target IL-17 cytokines in acute pancreatitis.

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Section: Therapeutic Implications Of Apmentioning

confidence: 99%

Role of Interleukin-17 in Acute Pancreatitis

Chen

Liu

et al. 2021

Front. Immunol.

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“…Lipopolysaccharide (LPS), a main component of bacterial cell walls, has been identified as a key factor in ALI development, which can trigger a rapid and robust inflammatory response and impair the normal function of immune cells, such as macrophages. Results from previous studies showed that continuous activation of macrophages was one of the key steps responsible for accelerating ALI progress [9] , [10] , [11] , [12] . Macrophages perform multiple functions at different stages of ALI through the production of pro-inflammatory mediators including chemokines and cytokines such as interleukin-6 (IL-6), interleukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) [13] , [14] , [15] .…”

Section: Introductionmentioning

confidence: 99%

“…Research efforts in the field of ALI have primarily focused on the innate immune system and have typically conceptually viewed ALI as a syndrome of hyper-inflammation. Emerging evidence indicates that dysregulation of cytokines in acute inflammation is a crucial step in mediating, amplifying, and perpetuating ALI processes [1] , [2] , [3] , [4] , [9] . Lipopolysaccharide (LPS), a main component of bacterial cell walls, has been identified as a key factor in ALI development, which can trigger a rapid and robust inflammatory response and impair the normal function of immune cells, such as macrophages.…”

Section: Introductionmentioning

confidence: 99%

MNK as a potential pharmacological target for suppressing LPS-induced acute lung injury in mice

Gao

Teng

Yang

et al. 2021

Biochemical Pharmacology

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“…Injection of LPS was widely used for induce lung injury in animals ( Li et al, 2020 ; Liu et al, 2020b ). However, injection with LPS causes the systemic inflammation and thus lacks tissue specificity ( Wang et al, 2020a ; Weng et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Berberine administrated with different routes attenuates inhaled LPS-induced acute respiratory distress syndrome through TLR4/NF-κB and JAK2/STAT3 inhibition

Wan

et al. 2021

European Journal of Pharmacology

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Accumulating evidence showed that berberine possessed the anti-inflammatory action in various diseases caused by inflammation. However, it was still unclear whether both inhalation and injection with berberine produced pulmonary protective role in acute respiratory distress syndrome (ARDS). This study was aimed to evaluate the effects of both administration routes including inhalation and injection with berberine in ARDS induced by lipopolysaccharide (LPS) inhalation. Histopathological examination and weight of lung were evaluated. Phosphorylation of NF-κB, JAK2 and STAT3 were measured to assess the activity of inflammation related signaling pathways. Proinflammatory cytokines including interleukin (IL)-1β and tumor necrosis factor (TNF)-α in the bronchoalveolar lavage fluid (BALF) and serum were also detected. The results showed that LPS caused the lung injury, while both administration routes with berberine attenuated the injury and improved the pulmonary morphology. In addition, the primary TLR4/NF-κB and secondary JAK2/STAT3 signaling pathways which were activated by LPS in lung were totally inhibited by berberine administration. Moreover, proinflammatory cytokines in both BALF and serum were decreased by berberine. Considering that molecular docking simulation indicated that berberine could bind with TLR4, the present suggested that the inhibition of the inflammation related TLR4/NF-κB and JAK2/STAT3 signaling pathways might be involved in the pulmonary protective effect of berberine in LPS-induced ARDS.

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Ellipticine blocks synergistic effects of IL-17A and TNF-α in epithelial cells and alleviates severe acute pancreatitis-associated acute lung injury

Cited by 27 publications

References 39 publications

Role of Interleukin-17 in Acute Pancreatitis

Role of Interleukin-17 in Acute Pancreatitis

MNK as a potential pharmacological target for suppressing LPS-induced acute lung injury in mice

Berberine administrated with different routes attenuates inhaled LPS-induced acute respiratory distress syndrome through TLR4/NF-κB and JAK2/STAT3 inhibition

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