Gallic acid against hepatocellular carcinoma: An integrated scheme of the potential mechanisms of action from<i>in vivo</i>study

Aglan, Hadeer A.; Ahmed, Hanaa H.; El‐Toumy, Sayed A.; Mahmoud, Nadia S.

doi:10.1177/1010428317699127

Cited by 34 publications

(25 citation statements)

References 49 publications

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“…It is generally believed that GA triggers cancer cells to die through apoptosis [20], which is a cell suicide process [21]. In the present study, we applied 50 µg/mL of GA to trigger cancer cell death, as in vivo studies demonstrated that administration of this dosage of GA is well-tolerated by animals, such as rats, without adverse physiological response detected [22,23]. This is also the concentration commonly used in the in vitro studies of GA to promote cancer cell death and other cellular responses [20,24,25].…”

Section: Resultsmentioning

confidence: 99%

Gallic Acid Triggers Iron-Dependent Cell Death with Apoptotic, Ferroptotic, and Necroptotic Features

Tang

Cheung

2019

Toxins

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Gallic acid (GA) is a natural anti-cancer compound that can be found in many food sources, including edible mushrooms, fruits, and vegetables. Studies generally attribute the anti-cancer activity of GA to the induction of apoptosis. Here, we reported that GA activated iron-dependent cell death mechanisms with apoptotic, ferroptotic, and necroptotic features. Our time-lapse live-cell microscopy study demonstrated that GA could induce coexistence of multiple types of cell death pathways, including apoptosis characterized by mitochondrial cytochrome c release and caspase-3 activation, ferroptosis characterized by lipid peroxidation, and necroptosis characterized by the loss of plasma membrane integrity. This GA-induced cell death could be completely suppressed by exposure to an iron chelator deferoxamine, indicating that it is an iron-dependent cell death process. Importantly, MLKL (mixed lineage kinase domain-like protein) inhibitor necrosulfonamide exerted a synergistic effect by increasing the sensitivity of cancer cells to GA. Taken together, our results provide new mechanistic insights, and also suggest new strategies to enhance the efficacy of this natural anti-cancer compound by identifying the agents that can promote or suppress the GA-induced cell death process.

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Section: Resultsmentioning

confidence: 99%

Gallic Acid Triggers Iron-Dependent Cell Death with Apoptotic, Ferroptotic, and Necroptotic Features

Tang

Cheung

2019

Toxins

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“…The strong antioxidant capacity of the Gordonia axillaris fruit might be attributed to the synergistic effect of these phenolic components, as well as other antioxidants. Besides, except for antioxidant capacity, these phenolic compounds have also shown other bioactivities, such as anticancer, anti-inflammatory and antibacterial activities [ 54 , 55 , 56 , 57 , 58 , 59 ], which indicated that the Gordonia axillaris fruit might possess these bioactivities.…”

Section: Resultsmentioning

confidence: 99%

Microwave-Assisted Extraction of Natural Antioxidants from the Exotic Gordonia axillaris Fruit: Optimization and Identification of Phenolic Compounds

Lin³

et al. 2017

Molecules

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Our previous study reported that the fruit of Gordonia axillaris, an edible wild fruit, possessed strong antioxidant activity. In this study, a microwave-assisted extraction (MAE) method was established to extract antioxidants from the fruit of Gordonia axillaris. The influence of five parameters, including ethanol concentration, solvent/material ratio, extraction time, extraction temperature and microwave power, was investigated by single-factor experiments. Three factors, namely ethanol concentration, solvent/material ratio, extraction time, were found to exert a major influence on extraction efficacy, and were further studied by response surface methodology to investigate their interactions. Ethanol concentration of 36.89%, solvent/material ratio of 29.56 mL/g, extraction time of 71.04 min, temperature of 40 °C, and microwave power of 400 W were found to be the optimal condition. The TEAC value was 198.16 ± 5.47 µmol Trolox/g DW under the optimal conditions, which was in conformity to the predicted value (200.28 µmol Trolox/g DW). In addition, the MAE method was compared with two conventional methods (Soxhlet extraction and maceration extraction). Results showed that the antioxidant capacity of the extract obtained by MAE method was stronger than that obtained by maceration (168.67 ± 3.88 µmol Trolox/g DW) or Soxhlet extraction (114.09 ± 2.01 µmol Trolox/g DW). Finally, several phenolic compounds in the extract were identified and quantified by UPLC-MS/MS, which were rutin, gallic acid, protocatechuic acid, epicatechin, epicatechin gallate, 2-hydrocinnamic acid, p-coumaric acid, quercetin, chlorogenic acid and ferulic acid.

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“…The parameters such as ALT, AST, γGT, MDA, IL-6, and TNF-α were significantly reduced [39]. In addition, gallic acid (50 mg/kg) for five weeks reduces N-ntrosodiethylamine- induced hepatocellular carcinoma owing to regulate signal transducer through antioxidant and anti-inflammatory effects [40]. Basis on these reports and our results, we suggest that the polyphenol-rich components of NLE potentially provide benefits for blocking AAF-induced hepatocarcinogenesis through enhancing antioxidative potential and alleviating inflammation.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory Effect of Nelumbo nucifera Leaf Extract on 2-Acetylaminofluorene-induced Hepatocarcinogenesis Through Enhancing Antioxidative Potential and Alleviating Inflammation in Rats

et al. 2019

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Leaf extract of Nelumbo nucifera (NLE) has been demonstrated to possess anti-atherosclerosis, improve alcohol-induced steatohepatitis, prevent high-fat diet-induced obesity, and inhibit the proliferation and metastasis of human breast cancer cells. This study determines the chemopreventive role of NLE against 2-acetylaminofluorene (AAF)-induced hepatocellular carcinoma (HCC) in rats. AAF was used to induce hepatocarcinogenesis in rats through genetic and nongenetic effects. After administration for 12 weeks, NLE (0.5–2%) supplementation orally inhibited AAF (0.03%)-induced hepatic fibrosis which appears during the development of premalignant lesions in rats. After the 6-month experiment, NLE supplementation resulted in decreasing AAF-induced serum parameters of hepatic injury, including the level of triglycerides, total cholesterol, alpha-fetoprotein (AFP), and inflammatory mediator interleukin (IL)-6 and tumor necrosis factor (TNF)-α as well as the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyl transferase (γGT). NLE supplementation also reduced AAF-induced lipid peroxidation and 8-hydroxy-2′-deoxyguanosine (8-OHdG) formation in the rat liver. Hepatic histopathological investigation revealed that NLE supplementation attenuated the AAF-induced HCC and glutathione S-transferase-Pi (GST-Pi) expression. Furthermore, NLE supplementation increased the expression of transcription factor, nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream targets, including catalase, glutathion peroxidase (GPx), and superoxide dismutase 1 (SOD-1) in the rat liver. Our findings indicate that NLE supplementation inhibited AAF-induced hepatocarcinogenesis by enhancing antioxidative potential and alleviating inflammation in rats.

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Gallic acid against hepatocellular carcinoma: An integrated scheme of the potential mechanisms of action fromin vivostudy

Cited by 34 publications

References 49 publications

Gallic Acid Triggers Iron-Dependent Cell Death with Apoptotic, Ferroptotic, and Necroptotic Features

Gallic Acid Triggers Iron-Dependent Cell Death with Apoptotic, Ferroptotic, and Necroptotic Features

Microwave-Assisted Extraction of Natural Antioxidants from the Exotic Gordonia axillaris Fruit: Optimization and Identification of Phenolic Compounds

Inhibitory Effect of Nelumbo nucifera Leaf Extract on 2-Acetylaminofluorene-induced Hepatocarcinogenesis Through Enhancing Antioxidative Potential and Alleviating Inflammation in Rats

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