Macrophages in pancreatitis: Mechanisms and therapeutic potential

Hu, Fenglin; Lou, Ni; Jiao, Juying; Guo, Fengjin; Xiang, Hong; Shang, Dong

doi:10.1016/j.biopha.2020.110693

Cited by 94 publications

(69 citation statements)

References 121 publications

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“…6,7) Furthermore, they can accelerate the inflammatory response by activating or increasing the expression of pro-inflammatory mediators as well as other pro-inflammatory cytokines. 8,39) In the current study, we found that loganin reduced the production of TNF-α and IL-1β in LPS-stimulated RAW264.7 macrophages by suppressing their expression. Consistent with our results, Cui et al 22) also reported similar effects in BV-2 microglia stimulated with amyloid β, and these results support the anti-inflammatory efficacy of loganin found in several experimental models.…”

Section: Discussionsupporting

confidence: 52%

“…18,22,28) Cytokines are secreted primary by macrophages in response to inflammation, which are involved in various signaling pathways producing autocrine and/or paracrine effects. [38][39][40] All of these are essential components for the initiation and improvement of the inflammatory response, and their expression is also increased by the LPS stimulation of macrophages. 6,7) Furthermore, they can accelerate the inflammatory response by activating or increasing the expression of pro-inflammatory mediators as well as other pro-inflammatory cytokines.…”

Section: Discussionmentioning

confidence: 99%

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Loganin Inhibits Lipopolysaccharide-Induced Inflammation and Oxidative Response through the Activation of the Nrf2/HO-1 Signaling Pathway in RAW264.7 Macrophages

Park

Lee

Kwon

et al. 2021

Biological & Pharmaceutical Bulletin

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Inflammation caused by the excessive secretion of inflammatory mediators in abnormally activated macrophages promotes many diseases along with oxidative stress. Loganin, a major iridoid glycoside isolated from Cornus officinalis, has recently been reported to exhibit anti-inflammatory and antioxidant effects, whereas the underlying mechanism has not yet been fully clarified. Therefore, the aim of the present study is to investigate the effect of loganin on inflammation and oxidative stress in lipopolysaccharide (LPS)stimulated RAW264.7 macrophages. Our results indicated that loganin treatment markedly attenuated the LPS-mediated phagocytic activity and release of nitric oxide (NO) and prostaglandin E 2 , which was associated with decreased the expression of inducible NO synthase and cyclooxygenase-2. In addition, loganin suppressed the expression and their extracellular secretion of LPS-induced pro-inflammatory cytokines, such as tumor necrosis factor-α and interleukin-1β. Furthermore, loganin abolished reactive oxygen species (ROS) generation, and promoted the activation of nuclear factor-E2-related factor 2 (Nrf2) and the expression of heme oxygenase-1 (HO-1) in LPS-stimulated macrophages. However, zinc protoporphyrin, a selective HO-1 inhibitor, reversed the loganin-mediated suppression of pro-inflammatory cytokines in LPS-treated macrophages. In conclusion, our findings suggest that the upregulation of the Nrf2/HO-1 signaling pathway is concerned at least in the protective effect of loganin against LPS-mediated inflammatory and oxidative stress, and that loganin can be a potential functional agent to prevent inflammatory and oxidative damage.

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Section: Discussionsupporting

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Loganin Inhibits Lipopolysaccharide-Induced Inflammation and Oxidative Response through the Activation of the Nrf2/HO-1 Signaling Pathway in RAW264.7 Macrophages

Park

Lee

Kwon

et al. 2021

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

show abstract

“…During the inflammatory response, macrophages secrete multiple pro-inflammatory cytokines that are involved in various signaling pathways producing autocrine and/or paracrine effects 48 , 49 . All of these are essential components for the initiation and improvement of the inflammatory response, and their expression is also increased by the LPS stimulation of muscle cells 3 , 4 , 50 .…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Lipopolysaccharide-Induced Inflammatory and Oxidative Responses by Trans-cinnamaldehyde in C2C12 Myoblasts

et al. 2021

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“…Furthermore, macrophages interact with neighboring cells in a cytokine-dependent manner to accelerate the formation of pancreatic fibrosis during pancreatitis [ 42 , 43 ]. Recent studies have shown that the oral administration of camostat mesilate (CM), a drug for CP treatment, reduces pancreatic fibrosis and subsequent inflammation by inhibiting the activity of monocytes [ 44 ]. In sum, macrophages, as the major infiltrating immune cells in the tumor microenvironment (TME), play an important role in pancreatic fibrosis and inflammation.…”

Section: The Role Of Fibrosis In Pancreatitismentioning

confidence: 99%

Targeting Fibrosis: The Bridge That Connects Pancreatitis and Pancreatic Cancer

Huang

Iovanna

Santofimia‐Castaño

2021

IJMS

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Pancreatic fibrosis is caused by the excessive deposits of extracellular matrix (ECM) and collagen fibers during repeated necrosis to repair damaged pancreatic tissue. Pancreatic fibrosis is frequently present in chronic pancreatitis (CP) and pancreatic cancer (PC). Clinically, pancreatic fibrosis is a pathological feature of pancreatitis and pancreatic cancer. However, many new studies have found that pancreatic fibrosis is involved in the transformation from pancreatitis to pancreatic cancer. Thus, the role of fibrosis in the crosstalk between pancreatitis and pancreatic cancer is critical and still elusive; therefore, it deserves more attention. Here, we review the development of pancreatic fibrosis in inflammation and cancer, and we discuss the therapeutic strategies for alleviating pancreatic fibrosis. We further propose that cellular stress response might be a key driver that links fibrosis to cancer initiation and progression. Therefore, targeting stress proteins, such as nuclear protein 1 (NUPR1), could be an interesting strategy for pancreatic fibrosis and PC treatment.

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Macrophages in pancreatitis: Mechanisms and therapeutic potential

Cited by 94 publications

References 121 publications

Loganin Inhibits Lipopolysaccharide-Induced Inflammation and Oxidative Response through the Activation of the Nrf2/HO-1 Signaling Pathway in RAW264.7 Macrophages

Loganin Inhibits Lipopolysaccharide-Induced Inflammation and Oxidative Response through the Activation of the Nrf2/HO-1 Signaling Pathway in RAW264.7 Macrophages

Inhibition of Lipopolysaccharide-Induced Inflammatory and Oxidative Responses by Trans-cinnamaldehyde in C2C12 Myoblasts

Targeting Fibrosis: The Bridge That Connects Pancreatitis and Pancreatic Cancer

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