Yangonin inhibits ethanol-induced hepatocyte senescence via miR-194/FXR axis

Dong, Renchao; Wang, Xiaohui; Wang, Lu; Wang, Changyuan; Huang, Kai; Fu, Ting; Liu, Kexin; Wu, Jingjing; Sun, Huijun; Meng, Qiang

doi:10.1016/j.ejphar.2020.173653

Cited by 14 publications

(7 citation statements)

References 53 publications

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“…Consistently, this research found that miR-194 was up-regulated in OGD-treated hepatocyte injury, and miR-194 overexpression restored the regulatory effect of DEX on apoptosis and inflammation in OGDinduced WRL-68 cells. In addition, miR-194 was overexpressed in patients with liver diseases, and Yangonin inhibited cell aging by regulating miR-194 and alleviated alcohol-induced liver injury [44]. Our research was similar to this study, indicating that miR-194 could be sponged by TUG1 in hepatocyte injury.…”

Section: Discussionsupporting

confidence: 84%

“…Meanwhile, miR-194 is known to be a crucial mediator in inflammatory responses [42,43]. Moreover, miR-194 could aggravate the liver injury [44]. Consistently, this research found that miR-194 was up-regulated in OGD-treated hepatocyte injury, and miR-194 overexpression restored the regulatory effect of DEX on apoptosis and inflammation in OGDinduced WRL-68 cells.…”

Section: Discussionsupporting

confidence: 66%

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Dexmedetomidine hydrochloride inhibits hepatocyte apoptosis and inflammation by activating the lncRNA TUG1/miR-194/SIRT1 signaling pathway

Xiao-hong

Liao

et al. 2021

J Inflamm

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Background Liver injury seriously threatens the health of people. Meanwhile, dexmedetomidine hydrochloride (DEX) can protect against liver injury. However, the mechanism by which Dex mediates the progression of liver injury remains unclear. Thus, this study aimed to investigate the function of DEX in oxygen and glucose deprivation (OGD)-treated hepatocytes and its underlying mechanism. Methods In order to investigate the function of DEX in liver injury, WRL-68 cells were treated with OGD. Cell viability was measured by MTT assay. Cell apoptosis was detected by flow cytometry. Inflammatory cytokines levels were measured by ELISA assay. The interaction between miR-194 and TUG1 or SIRT1 was detected by dual-luciferase reporter. Gene and protein levels were measured by qPCR or western blotting. Results DEX notably reversed OGD-induced inflammation and apoptosis in WRL-68 cell. Meanwhile, the effect of OGD on TUG1, SIRT1 and miR-194 expression in WRL-68 cells was reversed by DEX treatment. However, TUG1 knockdown or miR-194 overexpression reversed the function of DEX in OGD-treated WRL-68 cells. Moreover, TUG1 could promote the expression of SIRT1 by sponging miR-194. Furthermore, knockdown of TUG1 promoted OGD-induced cell growth inhibition and inflammatory responses, while miR-194 inhibitor or SIRT1 overexpression partially reversed this phenomenon. Conclusions DEX could suppress OGD-induced hepatocyte apoptosis and inflammation by mediation of TUG1/miR-194/SIRT1 axis. Therefore, this study might provide a scientific basis for the application of DEX on liver injury treatment.

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Section: Discussionsupporting

confidence: 84%

Section: Discussionsupporting

confidence: 66%

Dexmedetomidine hydrochloride inhibits hepatocyte apoptosis and inflammation by activating the lncRNA TUG1/miR-194/SIRT1 signaling pathway

Xiao-hong

Liao

et al. 2021

J Inflamm

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“…Our IF analysis revealed that PAR level was significantly increased in untreated aged mice but was exacerbated by chronic alcohol consumption in both young and aged mice ( Figure 4 A). In vitro assays have shown that senescence, a stress response that universally occurs within tissues under pathophysiological conditions, is stimulated in hepatocytes by ethanol, suggesting that it plays a key role in ALD [ 44 ]; moreover, in hepatocyte cultures exposed to ethanol the SA-β-gal activity, a widely used biomarker of cellular senescence, is increased [ 45 ]. Interestingly, our results showed that the activity of SA-β-gal was increased in untreated 18-month-old mice, but this increment was observed from 12 months on and potentiated in 18-month-old mice subjected to the ALD model ( Figure 4 B), indicating that chronic alcohol consumption exacerbated the appearance of senescent cells in the liver of aged mice.…”

Section: Discussionmentioning

confidence: 99%

Nucleoredoxin Redox Interactions Are Sensitized by Aging and Potentiated by Chronic Alcohol Consumption in the Mouse Liver

Idelfonso-García,

Alarcón-Sánchez,

Guerrero-Escalera

et al. 2024

Antioxidants

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Aging is characterized by increased reactive species, leading to redox imbalance, oxidative damage, and senescence. The adverse effects of alcohol consumption potentiate aging-associated alterations, promoting several diseases, including liver diseases. Nucleoredoxin (NXN) is a redox-sensitive enzyme that targets reactive oxygen species and regulates key cellular processes through redox protein–protein interactions. Here, we determine the effect of chronic alcohol consumption on NXN-dependent redox interactions in the liver of aged mice. We found that chronic alcohol consumption preferentially promotes the localization of NXN either into or alongside senescent cells, declines its interacting capability, and worsens the altered interaction ratio of NXN with FLII, MYD88, CAMK2A, and PFK1 proteins induced by aging. In addition, carbonylated protein and cell proliferation increased, and the ratios of collagen I and collagen III were inverted. Thus, we demonstrate an emerging phenomenon associated with altered redox homeostasis during aging, as shown by the declining capability of NXN to interact with partner proteins, which is enhanced by chronic alcohol consumption in the mouse liver. This evidence opens an attractive window to elucidate the consequences of both aging and chronic alcohol consumption on the downstream signaling pathways regulated by NXN-dependent redox-sensitive interactions.

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“…Yangonin is recently reported to exhibit antifibrotic action in TAA-induced live fibrosis model in mice, which is related with its anti-inflammatory effect and inhibition on activation of HSCs through activating FXR [15]. Moreover, yangonin also has hepatoprotection in alcohol or HFD-induced liver disease model in mice by activating FXR [310][311][312]. Furthermore, yangonin relieves ANIT, estrogen or lithocholic acid-induced cholestasis and hepatotoxicity via its anti-inflammatory effect, FXR activation, or modulation of hepatic transporters [313][314][315].…”

Section: Yangoninmentioning

confidence: 99%

“…Yangonin, a kavalactone (Fig. 4m), can be isolated from edible Kava in the South Pacific region [310]. Yangonin is recently reported to exhibit antifibrotic action in TAA-induced live fibrosis model in mice, which is related with its anti-inflammatory effect and inhibition on activation of HSCs through activating FXR [15].…”

Section: Yangoninmentioning

confidence: 99%

A review of edible plant-derived natural compounds for the therapy of liver fibrosis

Wang

Niu

et al. 2022

European Journal of Gastroenterology &Amp; Hepatology

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Liver fibrosis has a high incidence worldwide and is the common pathological basis of many chronic liver diseases. Liver fibrosis is caused by the excessive deposition of extracellular matrix and concomitant collagen accumulation in livers and can lead to the development of liver cirrhosis and even liver cancer. A large number of studies have provided evidence that liver fibrosis can be blocked or even reversed by appropriate medical interventions. However, the antifibrosis drugs with ideal clinical efficacy are still insufficient. The edible plant-derived natural compounds have been reported to exert effective antifibrotic effects with few side-effects, representing a kind of promising source for the treatment of liver fibrosis. In this article, we reviewed the current progress of the natural compounds derived from dietary plants in the treatment of liver fibrosis, including phenolic compounds (capsaicin, chlorogenic acid, curcumin, ellagic acid, epigallocatechin-3-gallate, resveratrol, sinapic acid, syringic acid, vanillic acid and vitamin E), flavonoid compounds (genistein, hesperidin, hesperetin, naringenin, naringin and quercetin), sulfur-containing compounds (S-allylcysteine, ergothioneine, lipoic acid and sulforaphane) and other compounds (betaine, caffeine, cucurbitacin B, lycopene, α-mangostin, γ-mangostin, ursolic acid, vitamin C and yangonin). The pharmacological effects and related mechanisms of these compounds in in-vivo and in-vitro models of liver fibrosis are focused.

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Yangonin inhibits ethanol-induced hepatocyte senescence via miR-194/FXR axis

Cited by 14 publications

References 53 publications

Dexmedetomidine hydrochloride inhibits hepatocyte apoptosis and inflammation by activating the lncRNA TUG1/miR-194/SIRT1 signaling pathway

Dexmedetomidine hydrochloride inhibits hepatocyte apoptosis and inflammation by activating the lncRNA TUG1/miR-194/SIRT1 signaling pathway

Nucleoredoxin Redox Interactions Are Sensitized by Aging and Potentiated by Chronic Alcohol Consumption in the Mouse Liver

A review of edible plant-derived natural compounds for the therapy of liver fibrosis

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