Gallic acid and ferulic acid protect the liver from thioacetamide-induced fibrosis in rats via differential expression of miR-21, miR-30 and miR-200 and impact on TGF-β1/Smad3 signaling

Hussein, Rasha M.; Anwar, Mona M; Farghaly, Hatem S.; Kandeil, Mohamed A.

doi:10.1016/j.cbi.2020.109098

Cited by 34 publications

(20 citation statements)

References 45 publications

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“…GA has been found to regulate various cellular pathways, such as the bone morphogenetic protein 2 (BMP2)-Smad1/5/8 signaling, 22 c-Jun N-terminal kinases 2 (JNK2) signaling, 23 TGF-β/Smad3 signaling, 24 and histone deacetylase 1 or histone deacetylase 2. 25 Its spectral anti-inflammatory function makes it clinically valuable.…”

Section: Discussionmentioning

confidence: 99%

Gallic Acid Ameliorates Atopic Dermatitis-Like Skin Inflammation Through Immune Regulation in a Mouse Model

Hu¹,

Zhou²

2021

CCID

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Section: Discussionmentioning

confidence: 99%

Gallic Acid Ameliorates Atopic Dermatitis-Like Skin Inflammation Through Immune Regulation in a Mouse Model

Hu¹,

Zhou²

2021

CCID

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“…However, Smad7, as an inhibitory Smad (I-Smad), may block the TGF- β 1/Smads signaling pathway by interfering with the activated TGF- β RI. This also means that the phosphorylation of Smad2/3 is hindered from the root cause, thereby delaying or improving the process of fibrosis [ 16 , 17 ]. Moreover, the screening of targets related to the TGF- β signaling pathway has become a novel method to provide theoretical support for the development of therapeutic drugs of fibrotic diseases [ 13 – 15 , 18 ].…”

Section: Molecular and Cellular Mechanisms Of Fibrosismentioning

confidence: 99%

Gasotransmitters: Potential Therapeutic Molecules of Fibrotic Diseases

Chen

Yuan

Cao

et al. 2021

Oxidative Medicine and Cellular Longevity

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Fibrosis is defined as the pathological progress of excessive extracellular matrix (ECM), such as collagen, fibronectin, and elastin deposition, as the regenerative capacity of cells cannot satisfy the dynamic repair of chronic damage. The well-known features of tissue fibrosis are characterized as the presence of excessive activated and proliferated fibroblasts and the differentiation of fibroblasts into myofibroblasts, and epithelial cells undergo the epithelial-mesenchymal transition (EMT) to expand the number of fibroblasts and myofibroblasts thereby driving fibrogenesis. In terms of mechanism, during the process of fibrosis, the activations of the TGF-β signaling pathway, oxidative stress, cellular senescence, and inflammatory response play crucial roles in the activation and proliferation of fibroblasts to generate ECM. The deaths due to severe fibrosis account for almost half of the total deaths from various diseases, and few treatment strategies are available for the prevention of fibrosis as yet. Recently, numerous studies demonstrated that three well-defined bioactive gasotransmitters, including nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H2S), generally exhibited anti-inflammatory, antioxidative, antiapoptotic, and antiproliferative properties. Besides these effects, a number of studies have reported that low-dose exogenous and endogenous gasotransmitters can delay and interfere with the occurrence and development of fibrotic diseases, including myocardial fibrosis, idiopathic pulmonary fibrosis, liver fibrosis, renal fibrosis, diabetic diaphragm fibrosis, and peritoneal fibrosis. Furthermore, in animal and clinical experiments, the inhalation of low-dose exogenous gas and intraperitoneal injection of gaseous donors, such as SNAP, CINOD, CORM, SAC, and NaHS, showed a significant therapeutic effect on the inhibition of fibrosis through modulating the TGF-β signaling pathway, attenuating oxidative stress and inflammatory response, and delaying the cellular senescence, while promoting the process of autophagy. In this review, we first demonstrate and summarize the therapeutic effects of gasotransmitters on diverse fibrotic diseases and highlight their molecular mechanisms in the process and development of fibrosis.

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“…Hussein et al [ 90 ] evaluated the effects of GA and FA against an experimentally induced liver fibrosis by thioacetamide (TAA). Supplementation of rats with both FA and GA at 20 mg/kg/day, for six weeks exhibited hepatoprotective and antioxidant effects against TAA-induced liver fibrosis (mediated through inhibition of TGF-β1/Smad3 signalling and differentially regulating the hepatic expression level of miR-21, miR-30 and miR-200).…”

Section: Biochemical and Health Properties Of The Examined Phenolic Acidsmentioning

confidence: 99%

A Review of the Health Protective Effects of Phenolic Acids against a Range of Severe Pathologic Conditions (Including Coronavirus-Based Infections)

Kiokias

Oreopoulou

2021

Molecules

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Phenolic acids comprise a class of phytochemical compounds that can be extracted from various plant sources and are well known for their antioxidant and anti-inflammatory properties. A few of the most common naturally occurring phenolic acids (i.e., caffeic, carnosic, ferulic, gallic, p-coumaric, rosmarinic, vanillic) have been identified as ingredients of edible botanicals (thyme, oregano, rosemary, sage, mint, etc.). Over the last decade, clinical research has focused on a number of in vitro (in human cells) and in vivo (animal) studies aimed at exploring the health protective effects of phenolic acids against the most severe human diseases. In this review paper, the authors first report on the main structural features of phenolic acids, their most important natural sources and their extraction techniques. Subsequently, the main target of this analysis is to provide an overview of the most recent clinical studies on phenolic acids that investigate their health effects against a range of severe pathologic conditions (e.g., cancer, cardiovascular diseases, hepatotoxicity, neurotoxicity, and viral infections—including coronaviruses-based ones).

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Gallic acid and ferulic acid protect the liver from thioacetamide-induced fibrosis in rats via differential expression of miR-21, miR-30 and miR-200 and impact on TGF-β1/Smad3 signaling

Cited by 34 publications

References 45 publications

Gallic Acid Ameliorates Atopic Dermatitis-Like Skin Inflammation Through Immune Regulation in a Mouse Model

Gallic Acid Ameliorates Atopic Dermatitis-Like Skin Inflammation Through Immune Regulation in a Mouse Model

Gasotransmitters: Potential Therapeutic Molecules of Fibrotic Diseases

A Review of the Health Protective Effects of Phenolic Acids against a Range of Severe Pathologic Conditions (Including Coronavirus-Based Infections)

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