Anthocyanins isolated from blueberry ameliorates CCl4 induced liver fibrosis by modulation of oxidative stress, inflammation and stellate cell activation in mice

Sun, Jianchao; Wu, Yafeng; Long, Cuizhen; He, Ping; Gu, Junjie; Yang, Lei; Liang, Yao-Dong; Wang, Yuping

doi:10.1016/j.fct.2018.07.048

Cited by 78 publications

(58 citation statements)

References 50 publications

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“…Inflammation is directly linked to liver fibrosis, and suppressing inflammation can effectively control liver fibrosis. We herein studied the effects of celastrol on the levels of inflammatory factors in liver and serum of rats.…”

Section: Resultsmentioning

confidence: 99%

“…Compelling evidence linked inflammation to the development of liver fibrosis . Currently, few effective drugs can be used to treat liver fibrosis, and suppressing liver inflammation is an effective strategy to control liver fibrosis .…”

Section: Introductionmentioning

confidence: 99%

“…Compelling evidence linked inflammation to the development of liver fibrosis. 1,2 Currently, few effective drugs can be used to treat liver fibrosis, and suppressing liver inflammation is an effective strategy to control liver fibrosis. 3 It is well known that hepatic stellate cells (HSCs) activation is regarded as a critical step in mediating liver fibrosis, 4 and however, continuous secretion of inflammatory cytokines in liver tissue will lead to the persistent activation of HSCs.…”

Section: Introductionmentioning

confidence: 99%

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Celastrol exerts anti‐inflammatory effect in liver fibrosis via activation of AMPK‐SIRT3 signalling

Wang

et al. 2019

J Cellular Molecular Medi

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Celastrol, a pentacyclic tritepene extracted from Tripterygium Wilfordi plant, showing potent liver protection effects on several liver‐related diseases. However, the anti‐inflammatory potential of celastrol in liver fibrosis and the detailed mechanisms remain uncovered. This study was to investigate the anti‐inflammatory effect of celastrol in liver fibrosis and to further reveal mechanisms of celastrol‐induced anti‐inflammatory effects with a focus on AMPK‐SIRT3 signalling. Celastrol showed potent ameliorative effects on liver fibrosis both in activated hepatic stellate cells (HSCs) and in fibrotic liver. Celastrol remarkably suppressed inflammation in vivo and inhibited the secretion of inflammatory factors in vitro. Interestingly, celastrol increased SIRT3 promoter activity and SIRT3 expression both in fibrotic liver and in activated HSCs. Furthermore, SIRT3 silencing evidently ameliorated the anti‐inflammatory potential of celastrol. Besides, we found that celastrol could increase the AMPK phosphorylation. Further investigation showed that SIRT3 siRNA decreased SIRT3 expression but had no obvious effect on phosphorylation of AMPK. In addition, inhibition of AMPK by employing compound C (an AMPK inhibitor) or AMPK1α siRNA significantly suppressed SIRT3 expression, suggesting that AMPK was an up‐stream protein of SIRT3 in liver fibrosis. We further found that depletion of AMPK significantly attenuated the inhibitory effect of celastrol on inflammation. Collectively, celastrol attenuated liver fibrosis mainly through inhibition of inflammation by activating AMPK‐SIRT3 signalling, which makes celastrol be a potential candidate compound in treating or protecting against liver fibrosis.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Celastrol exerts anti‐inflammatory effect in liver fibrosis via activation of AMPK‐SIRT3 signalling

Wang

et al. 2019

J Cellular Molecular Medi

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“…42 Carbon tetrachloride (CCl 4 ) can accumulate a significant amount of Col-III in mouse liver. 43 Increasing expressions of Col-I and Col-III are related to hepatic fibrosis 44 and bile duct ligation. 45 Our results showed that Nano NiO could induce collagen deposition by histopathological examination and upregulate the contents of Col-I and Col-III in rat liver, which suggested that the hepatic fibrosis model was established in rats.…”

Section: Nano Nio Induced Hepatic Fibrosis In Ratsmentioning

confidence: 99%

TGF‐β1 mediated Smad signaling pathway and EMT in hepatic fibrosis induced by Nano NiO in vivo and in vitro

Zhang

Chang

Wang

et al. 2019

Environmental Toxicology

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Nickel oxide nanoparticles (Nano NiO) bears hepatotoxicity, while whether it leads to liver fibrosis remains unclear. The aim of this study was to establish the Nano NiO‐induced hepatic fibrosis model in vivo and investigate the roles of transforming growth factor β1 (TGF‐β1) in Smad pathway activation, epithelial‐mesenchymal transition (EMT) occurrence, and extracellular matrix (ECM) deposition in vitro. Male Wistar rats were exposed to 0.015, 0.06, and 0.24 mg/kg Nano NiO by intratracheal instilling twice a week for 9 weeks. HepG2 cells were treated with 100 μg/mL Nano NiO and TGF‐β1 inhibitor (SB431542) to explore the mechanism of collagen formation. Results of Masson staining as well as the elevated levels of type I collagen (Col‐I) and Col‐III suggested that Nano NiO resulted in hepatic fibrosis in rats. Furthermore, Nano NiO increased the protein expression of TGF‐β1, p‐Smad2, p‐Smad3, alpha‐smooth muscle actin (α‐SMA), matrix metalloproteinase9 (MMP9), and tissue inhibitors of metalloproteinase1 (TIMP1), while decreased the protein content of E‐cadherin and Smad7 in rat liver and HepG2 cells. Most importantly, Nano NiO‐triggered the abnormal expression of the abovementioned proteins were all alleviated by co‐treatment with SB431542, implying that TGF‐β1‐mediated Smad pathway, EMT and MMP9/TIMP1 imbalance were involved in overproduction of collagen in HepG2 cells. In conclusion, these findings indicated that Nano NiO induced hepatic fibrosis via TGF‐β1‐mediated Smad pathway activation, EMT occurrence, and ECM deposition.

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“…Natural antioxidants from fruits offer an alternative source of dietary ingredients to promote healthy life. In vivo studies show that epigallocatechin gallate contained in green tea is able to inhibit memory deficits in Alzheimer case [1], hesperidin isolated from citrus peels allows the regeneration of ulcerated tissue and prevents hemorrhagic injury of gastric mucosa [2], polyphenols in cocoa bean can reduce the risk of atherosclerosis [3], anthocyanins isolated from blueberry exhibits protection on liver [4], xanthones in mangosteen can protect nervous system [5], flavonoids of polymethoxylated flavones, procyanidins and isoflavones tyrosinase in several extracts (tangerine peels, cocoa and red clover) is potent to treat Parkinson's disease [6], and so forth. Basically, the assessment on antioxidant activity of plant extracts has lately received great attention.…”

Section: Introductionmentioning

confidence: 99%

Design of kaffir lime peel extract tablets by direct compression: Effects of filler-binder on rheological properties

Irawaty

Hadisoewignyo

Wijaya

et al. 2019

EXPLORING RESOURCES, PROCESS AND DESIGN FOR SUSTAINABLE URBAN DEVELOPMENT: Proceedings of the 5th International Conference on E

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Dried kaffir lime peels from Citrus hystrix were extracted with ethanol by maceration method, followed by solvent evaporation to obtain dry extract. Due to economical aspect and good flow properties of the extract, a direct compression method was applied in making the tablets. The main objective of this study was to study the influence of filler-binder (Avicel PH 102, Emcompress and Lactose) on rheological properties of kaffir lime peel extract tablet dough. Firstly, kaffir lime peel extract was prepared by peeling, cutting and drying kaffir lime peels prior to soaking them to ethanol. After separating the solid part, the extract was subsequently concentrated and filler was added into the crude extract to obtain dry product. Secondly, dry extract was then combined with filler-binder, sweetener and lubricant prior to the compression. Rheological properties evaluated in this study were density, flow time, the Carr index and the Hausner ratio. Thirdly, the best formulation dough was compressed to produce tablets. From the results, it can be concluded that ethanol is the best solvent to extract polyphenols from kaffir lime peels. In addition, the use of a mixture of lactose and Avicel PH 102 as the filler-binder agent exhibited the best formulation.

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Anthocyanins isolated from blueberry ameliorates CCl4 induced liver fibrosis by modulation of oxidative stress, inflammation and stellate cell activation in mice

Cited by 78 publications

References 50 publications

Celastrol exerts anti‐inflammatory effect in liver fibrosis via activation of AMPK‐SIRT3 signalling

Celastrol exerts anti‐inflammatory effect in liver fibrosis via activation of AMPK‐SIRT3 signalling

TGF‐β1 mediated Smad signaling pathway and EMT in hepatic fibrosis induced by Nano NiO in vivo and in vitro

Design of kaffir lime peel extract tablets by direct compression: Effects of filler-binder on rheological properties

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