Antifibrotic Compounds from &lt;i&gt;Liriodendron tulipifera&lt;/i&gt; Attenuating HSC-T6 Proliferation and TNF-α Production in RAW264.7 Cells

Jeong, Eun Ju; Kim, Nahyun; Heo, Jeong‐Doo; Lee, Ki Yong; Rho, Jung‐Rae; Kim, Young Choong; Sung, Sang Hyun

doi:10.1248/bpb.b14-00583

Cited by 13 publications

(9 citation statements)

References 44 publications

(33 reference statements)

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“…The second target involves antagonising the inflammatory cytokines released from hepatic macrophages, such as IL-1 and TNF-α, 41 or promoting the apoptosis of activated HSCs, thereby attenuating hepatic fibrosis. 42 43 …”

Section: Introductionmentioning

confidence: 99%

Hepatic macrophages in liver fibrosis: pathogenesis and potential therapeutic targets

You

et al. 2016

BMJ Open Gastroenterol

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Hepatic macrophages account for the largest non-parenchymal cell population in the liver. Recent studies have found that hepatic macrophages have different functions in different stages of experimental liver fibrosis. Some studies found that there are different types of hepatic macrophages in the liver, although others have suggested that hepatic macrophages could switch to different phenotypes in different environments. Many studies demonstrated that while hepatic macrophages promoted fibrosis through the recruitment of proinflammatory immune cells, and the secretion of proinflammatory cytokines and chemokines in the early stages, these also promoted the resolution of hepatic fibrosis through the secretion of matrix metalloproteinases in the late stages. This article will review the current role played by hepatic macrophages in liver fibrosis and the potential therapeutic targets that modulate hepatic macrophages.

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Section: Introductionmentioning

confidence: 99%

Hepatic macrophages in liver fibrosis: pathogenesis and potential therapeutic targets

You

et al. 2016

BMJ Open Gastroenterol

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“…Supernatant cultures of Lactobacillus kefiri BCRC14011, Lactobacillus kefiranofaciens BCRC16059, L. kefiranofaciens M1, L. kefiri M2, Leuconostoc mesenteroides M3, and Lactococcus lactis M4 can increase macrophage expression of IL-12, IL-6, IL-1β, and TNF-α in macrophages in vitro, and have strong *refers to the comparison between cells in the cell control group not exposed to any treatment and other groups exposed to different concentrations of SQ0048 without inhibitor treatment; it also refers to the comparison between groups without inhibitors and corresponding groups with inhibitors at the same concentration of SQ0048; # refers to the comparison between cells in the inhibitor control group with inhibitors but not SQ0048 and other groups with inhibitors. antibacterial activity (31). L. crispatus and L. iners can increase expression of IL-6, IL-8, and TNF-α (32).…”

Section: Discussionmentioning

confidence: 99%

Effect of Lactobacillus johnsonii Strain SQ0048 on the TLRs-MyD88/NF-κB Signaling Pathway in Bovine Vaginal Epithelial Cells

Cheng

Zhang²,

et al. 2021

Front. Vet. Sci.

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Vaginal inflammation is a common disease of the dairy cows' reproductive tract. Lactic acid bacteria can combat purulent inflammation caused by pathogenic bacteria and regulate the NF-κB signaling pathway mediated by toll-like receptors (TLRs) in the inflammatory response. We studied the effect of Lactobacillus johnsonii SQ0048, an isolate with antibacterial activity, on the NF-κB signaling pathway in cow vaginal epithelial cells. The expression levels of serial effectors related to the TLRs-MyD88/NF-κB signaling pathway (TLR2, TLR4, MyD88, IKK, NF-κB, IL-1β, IL-6, TNF-α, and IL-10) were measured with real-time polymerase chain reaction (RT-PCR), ELISA, and Western blot analyses. TLR2 and TLR4 were activated by SQ0048 cells, as noted by increased mRNA expression levels of TLR2 and TLR4 in SQ0048-treated bovine vaginal epithelial cells relative to control cells (P <0.01). SQ0048 treatment also significantly increased MyD88 and IKK expression, and activated NF-κB in vaginal epithelial cells (P <0.01). In addition, SQ0048 treatment also significantly increased mRNA expression levels of IL-1β, IL-6, and TNF-α, but decreased IL-10 mRNA expression levels (P <0.01). These data indicate that strain SQ0048 presence can improve the immune functions of cow vaginal epithelial cells by activating TLRs-MyD88/NF-κB signaling pathways. However, further in vivo studies are required to confirm these findings.

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“…The pathogenesis of liver fibrosis is very complex. Liver damage caused by virus, drug and other factor can stimulate macrophages to release inflammatory cytokines, these cytokines can participate in the production and degradation of extracellular collagen, and the activation and apoptosis of hepatic stellate cell through a variety of ways ( 22 ), which eventually leads to fibrosis. It has been found that H 2 S can promote apoptosis of vascular smooth muscle cells by downregulating the level of apoptosis inhibitors such as Bcl-2 and NF-κB ( 23 ).…”

Section: Discussionmentioning

confidence: 99%

The content of hydrogen sulfide in plasma of cirrhosis rats combined with portal hypertension and the correlation with indexes of liver function and liver fibrosis

Wei

Wang

2017

Exp Ther Med

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The purpose of this study is to investigate the content of hydrogen sulfide (H2S) in plasma of cirrhosis rats combined with portal hypertension and the correlation with indexes of liver function and liver fibrosis. Thirty female Sprague-Dawley rats were randomly divided into normal control group (NC), liver cirrhosis group (LC) and cirrhosis + propargylglycine (PPG) group (LC+PPG). Cirrhosis and portal hypertension were induced by carbon tetrachloride. Rats in LC+PPG group were intraperitoneally injected with H2S synthase inhibitor PPG for one week. Portal vein catheterization was used to measure portal vein pressure (PVP), and plasma H2S content was determined by deproteinization. Liver function was measured by automatic biochemical analyzer, and the fibrosis index was determined by radioimmunoassay. Real-time PCR was used to detect the expression levels of type I and type III collagen mRNA in liver tissue. Compared with NC group, levels of plasma H2S were significantly decreased (P<0.01), while PVP, alanine aminotransferase (ALT), aspartate aminotransferase (AST), laminin (LN), hyaluronic acid (HA), and expression levels of type III procollagen (PC III) and type I and type III collagen mRNAs were significantly increased in LC and LC+PPG groups (P<0.01). Compared with LC group, levels of plasma H2S were significantly decreased (P<0.01), while PVP, ALT, AST, LN, HA, and expression levels of PC III and type I and type III collagen mRNAs in LC+PPG group (P<0.05 or P<0.01). In conclusion, level of H2S was decreased and PVP was increased in cirrhosis rats, and H2S has the function of protecting liver function and anti-fibrosis.

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Antifibrotic Compounds from <i>Liriodendron tulipifera</i> Attenuating HSC-T6 Proliferation and TNF-α Production in RAW264.7 Cells

Cited by 13 publications

References 44 publications

Hepatic macrophages in liver fibrosis: pathogenesis and potential therapeutic targets

Hepatic macrophages in liver fibrosis: pathogenesis and potential therapeutic targets

Effect of Lactobacillus johnsonii Strain SQ0048 on the TLRs-MyD88/NF-κB Signaling Pathway in Bovine Vaginal Epithelial Cells

The content of hydrogen sulfide in plasma of cirrhosis rats combined with portal hypertension and the correlation with indexes of liver function and liver fibrosis

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