Gallic acid reduces cell growth by induction of apoptosis and reduction of IL-8 in HepG2 cells

Lima, Kelly Goulart; Krause, Gabriele Catyana; Schuster, Aline Daniele; Catarina, Anderson Velasque; Basso, Bruno Souza; Mesquita, Fernanda Cristina de; Pedrazza, Leonardo; Marczak, Elisa Simon; Martha, Bianca Andrade; Nunes, Fernanda Bordignon; Filippi-Chiela, Eduardo Cremonese; Jaeger, Natália; Thomé, Marcos Paulo Machado; Haute, Gabriela Viegas; Dias, Henrique Bregolin; Donadio, Márcio Vinı́cius Fagundes; Oliveira, Jarbas Rodrigues de

doi:10.1016/j.biopha.2016.10.048

Cited by 51 publications

(25 citation statements)

References 30 publications

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“…This may also explain the hormetic effect of AgNP in stimulating THP1 cell proliferation (Yusuf and Casey, 2019)and in HepG2 and A549 cancer cells (Jiao et al, 2014;Sthijns et al, 2017). Interestingly, HepG2 cell proliferation have been shown in another study to be inhibited by gallic acid through inhibition of IL-8 secretion (Lima et al, 2016), highlighting the possible contribution of AgNP-induced IL=8 secretion to cancer cell proliferation. Although, IL-1β release in the AgNP-exposed TDMs was significantly less than in AgNP-exposed THP1 monocytes, LPS priming of the TDM alone or with ATP stimulation resulted in IL-1β release comparable to that exhibited by the monocytic cell even under caspase-1 inhibition indicating no effect of AgNP or Lipo-AgNP on IL-1β release.…”

Section: Discussionmentioning

confidence: 89%

Surface modification of silver nanoparticle (AgNP) by liposomal encapsulation mitigates AgNP-induced inflammation

Yusuf

Casey

2019

Toxicology in Vitro

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Silver nanoparticles (AgNP) are widely used in a variety of consumable products as antibacterial to prevent or treat infection. Unfortunately, evidence exits that AgNP induces inflammation which can worsen with repeated human exposure. However, there is little or no research on how to mitigate these adverse effects due to AgNP induced-toxicity. Here, we investigated if surface modification of AgNP by liposomal encapsulation suppresses AgNP-mediated inflammatory responses in THP1 monocytes and THP1 differentiated macrophages (TDM). AgNP was encapsulated in a dipalmitoyl phosphatidyl choline-(DPPC)/cholesterol-based liposome by extrusion through a 100-nm polycarbonate membrane to form Lipo-AgNP. It was found as expected that AgNP induced significant release of IL-1β, IL-6, IL-8 and TNF-α in THP1 monocytes more than the basal level. Interestingly, release of these cytokines was suppressed by Lipo-AgNP. In TDMs, AgNP and Lipo-AgNP induced IL-8 release (p < .0001), but Lipo-AgNP maintained IL-8 release at levels significantly lower than that of AgNP (p < .01). However, both AgNP and Lipo-AgNP suppressed IL-1β and TNF-α release in LPS-stimulated THP1 monocytes and LPS-stimulated or unstimulated TDM respectively. We finally showed that Lipo-AgNP inhibits STAT-3 and this may be responsible for regulating the uncontrolled inflammation induced by AgNP likely mediated STAT-3 protein expression in LPS stimulated THP1 monocytes and TDMs, both LPS-stimulated and unstimulated. This data showed that Lipo-AgNP suppressed AgNP induced inflammation, making Lipo-AgNP particularly useful in treatment of bacteria induced inflammatory diseases and inflammatory cancers.

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Section: Discussionmentioning

confidence: 89%

Surface modification of silver nanoparticle (AgNP) by liposomal encapsulation mitigates AgNP-induced inflammation

Yusuf

Casey

2019

Toxicology in Vitro

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“…An Annexin V-FITC apoptosis detection kit was used to detect apoptotic cells using flow cytometry according to the manufacturer's instructions [ 25 ]. Cells in a six-well plate were pretreated with various drugs, the medium was aspirated, and the cells were washed once with PBS.…”

Section: Methodsmentioning

confidence: 99%

Ethyl Acetate Fraction of Hemerocallis citrina Baroni Decreases Tert‐butyl Hydroperoxide‐Induced Oxidative Stress Damage in BRL‐3A Cells

Wang

Hou

et al. 2018

Oxidative Medicine and Cellular Longevity

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The main purposes of this study were to screen the antioxidant activities of various fractions of Hemerocallis citrina Baroni and test their hepatoprotective effects in vitro. Antioxidant assays (2,2-diphenyl-1-picrylhydrazyl (DPPH), 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS), and reducing power experiments) and tert-butyl hydroperoxide- (t-BHP-) induced BRL-3A oxidative damage experiments were performed in vitro. The H. citrina ethyl acetate fraction (HCEA) was determined to have strong antioxidant activity because of its high flavonoid and polyphenol content. Ultraperformance liquid chromatography- (UPLC-) photodiode array (PDA)/mass spectrometry (MS) analysis showed that the main components of the HCEA were flavonoids and caffeic acid derivatives. A total of 17 compounds were identified. HCEA also effectively protected the liver against t-BHP-induced oxidative stress injury and significantly reduced reactive oxygen (ROS) accumulation. Moreover, HCEA significantly reduced levels of alanine aminotransferase (ALT), aspartate transaminase (AST), and lactate dehydrogenase (LDH). Further studies have shown that HCEA inhibits t-BHP-induced apoptosis by increasing B-cell lymphoma-2 (BCL-2) activity and decreasing caspase-3 and caspase-9 activity. Moreover, HCEA enhanced the activity of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT), as well as the total antioxidant capacity (T-AOC), and increased the antioxidant level of glutathione (GSH) in BRL-3A cells. HCEA increased the antioxidant capacity of cells by increasing the gene expression of AMP-activated protein kinase (AMPK), extracellular signal-regulated kinase (ERK), P38, nuclear factor, erythroid 2 like 2 (Nrf2), SOD, glutamate-cysteine ligase catalytic subunit (GCLC), glutamate-cysteine ligase modifier subunit (GCLM), and heme oxygenase 1 (HO-1), which are associated with antioxidant pathways to protect against oxidative stress. In conclusion, HCEA protected BRL-3A cells against t-BHP-induced oxidative stress damage via antioxidant and antiapoptosis pathways. Therefore, H. citrina Baroni may serve as a potential hepatoprotective drug.

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“…The apoptotic cells were identified by flow cytometry by using an Annexin V-FITC apoptosis detection kit in accordance with the manufacturer's instructions [ 26 ]. Briefly, HepG2 cells were seeded at a density of 5 × 10 4 cells/well into 6-well plates (2 mL/well).…”

Section: Methodsmentioning

confidence: 99%

Active Fragment of Veronica ciliata Fisch. Attenuates t‐BHP‐Induced Oxidative Stress Injury in HepG2 Cells through Antioxidant and Antiapoptosis Activities

Sun

et al. 2017

Oxidative Medicine and Cellular Longevity

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Excessive amounts of reactive oxygen species (ROS) in the body are a key factor in the development of hepatopathies such as hepatitis. The aim of this study was to assess the antioxidation effect in vitro and hepatoprotective activity of the active fragment of Veronica ciliata Fisch. (VCAF). Antioxidant assays (DPPH, superoxide, and hydroxyl radicals scavenging) were conducted, and hepatoprotective effects through the application of tert-butyl hydroperoxide- (t-BHP-) induced oxidative stress injury in HepG2 cells were evaluated. VCAF had high phenolic and flavonoid contents and strong antioxidant activity. From the perspective of hepatoprotection, VCAF exhibited a significant protective effect on t-BHP-induced HepG2 cell injury, as indicated by reductions in cytotoxicity and the levels of ROS, 8-hydroxydeoxyguanosine (8-OHdG), and protein carbonyls. Further study demonstrated that VCAF attenuated the apoptosis of t-BHP-treated HepG2 cells by suppressing the activation of caspase-3 and caspase-8. Moreover, it significantly decreased the levels of ALT and AST, increased the activities of acetyl cholinesterase (AChE), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT), and increased total antioxidative capability (T-AOC). Collectively, we concluded that VCAF may be a considerable candidate for protecting against liver injury owing to its excellent antioxidant and antiapoptosis properties.

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Gallic acid reduces cell growth by induction of apoptosis and reduction of IL-8 in HepG2 cells

Cited by 51 publications

References 30 publications

Surface modification of silver nanoparticle (AgNP) by liposomal encapsulation mitigates AgNP-induced inflammation

Surface modification of silver nanoparticle (AgNP) by liposomal encapsulation mitigates AgNP-induced inflammation

Ethyl Acetate Fraction of Hemerocallis citrina Baroni Decreases Tert‐butyl Hydroperoxide‐Induced Oxidative Stress Damage in BRL‐3A Cells

Active Fragment of Veronica ciliata Fisch. Attenuates t‐BHP‐Induced Oxidative Stress Injury in HepG2 Cells through Antioxidant and Antiapoptosis Activities

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