Evidence of similar protective effects afforded by white tea and its active component ‘EGCG’ on oxidative-stress mediated hepatic dysfunction during benzo(a)pyrene induced toxicity

Rangi, Sangeeta; Dhatwalia, Sunil Kumar; Bhardwaj, Priti; Kumar, Manoj; Dhawan, D. K.

doi:10.1016/j.fct.2018.04.044

Cited by 24 publications

(20 citation statements)

References 53 publications

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“…Benzo(α)pyrene (BaP), a major compound of the polycyclic aromatic hydrocarbon family (PAH), is recognized as a potent carcinogen with forceful immunotoxicity and reproduction toxicity (Yuan et al, 2017). It is ubiquitous in foods and ambient air, as a result of incomplete combustion of carbon compounds (Rangi et al, 2018). BaP is found in oils and fatty foods which are charcoal-broiled, grilled, baked, or smoked with these oils (Kazerouni et al, 2001;Lewtas, 2007).…”

Section: Introductionmentioning

confidence: 99%

Benzo[a]pyrene induces pyroptotic and autophagic death through inhibiting PI3K/Akt signaling pathway in HL-7702 human normal liver cells

Gao

Deng

et al. 2019

J. Toxicol. Sci.

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-Benzo(α)pyrene (BaP) possesses a forceful hepatotoxicity, and is ubiquitous in foods and ambient air. Our previous study found that BaP induced pyroptotic and autophagic death in HL-7702 human liver cells; the relevant mechanisms, however, remain unknown. This work was therefore to unravel the effects of the PI3K/Akt signaling pathway on pyroptotic and autophagic death triggered by BaP. Cells were treated with or without LY294002 (PI3K/Akt inhibitor) and IGF-1 (PI3K/Akt activator) before BaP exposure, and the results showed that compared with the control, the protein expression of p-Akt was markedly decreased by BaP (p < 0.05). IGF-1 did not subvert this inhibitive effect of BaP, while LY294002 enhanced it. Furthermore, the protein expression of pyroptosis (Cleaved Caspase-1, NO, IL-1β, IL-18), as well as LDH and the relative electrical conductivity were significantly augmented by BaP. The levels of these indices were increased by LY294002 pretreatment, and decreased by IGF-1. Similarly, LY294002 enhanced BaP-induced increase in the key protein expression of autophagy (Beclin-1 and LC3II), while IGF-1 weakened it. Finally, the phosphorylation of FOXO4 was clearly (p < 0.01) inhibited by BaP, and LY294002 suppressed this inhibitive effect of BaP, while IGF-1 strengthened it. In conclusion, BaP was able to induce pyroptotic and autophagic death via blocking the PI3K/Akt signaling pathway in HL-7702 liver cells.

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Section: Introductionmentioning

confidence: 99%

Benzo[a]pyrene induces pyroptotic and autophagic death through inhibiting PI3K/Akt signaling pathway in HL-7702 human normal liver cells

Gao

Deng

et al. 2019

J. Toxicol. Sci.

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“…MDA is the product of lipid peroxidation (Zhuang et al, 2016), H 2 O 2 is produced as a natural byproduct of the normal of oxygen and possesses strong oxidizing properties and causes the deleterious physiological effects (Debnath et al, 2018). It has reported that EGCG inhibited the BaP-induced oxidative damage by increasing the enzymes activities of T-SOD and GSH-px and reducing the level of MDA (Rangi, Dhatwalia, Bhardwaj, Kumar, & Dhawan, 2018). In the present investigation, we found that ISO overturned the reduction of activities of T-SOD and GSH-px and down-regulated the levels of MDA and H 2 O 2 induced by BaP (Figure 7) .…”

Section: Discussionmentioning

confidence: 99%

Isoorientin attenuates benzo[a]pyrene-induced liver injury by inhibiting autophagy and pyroptosis in vitro and vivo

Gao

et al. 2019

Food and Agricultural Immunology

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Benzo[a]pyrene (BaP), a carcinogen, leads to the severe liver injury. Isoorientin (ISO), a natural flavonoid, is known for its bioactivities, including anti-oxidation, anti-inflammation, and so on. However, there is no report on the effects of ISO on liver injury induced by BaP. The present study demonstrated that ISO treatment could relieve BaP-caused autophagic and pyroptotic injury in HL-7702 human hepatocyte and male BALB/c mice by down-regulating the numbers of autophagosomes, the mRNA expression of LC3 II and Beclin-1, and the levels of pyroptotic characteristic indices. Histopathology stained also confirmed that ISO could suppress the BaP-induced liver injury. Meanwhile, ISO was able to improve the liver function, and remarkably (p < 0.01) ameliorate hepatic oxidative injury by enhancing antioxidant enzymes activities (T-SOD, GSH-px) and reducing the levels of MDA and H 2 O 2. In conclusion, ISO possesses the positive inhibitive effects on BaPinduced the autophagic and pyroptotic liver injury in vitro and vivo.

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“…The hepato-protective effect of tea against chemical-induced liver injury was also demonstrated in several in vivo studies. White tea extract and the comparative dose of EGCG showed equivalent protective effects to attenuate benzo(a) pyrene-induced hepatic dysfunctions, in terms of increased biomarkers regarding inflammatory and oxidative stresses, decreased endogenous antioxidants, and the hepatic histoarchitectural alteration [172]. In addition, green tea could protect rats from alcohol-induced mitochondrial DNA damage, and could ameliorate oxidative stress by improving the activities of SOD, GPX, and CAT as well as increasing the content of GSH [173].…”

Section: Hepato-protective Effect In Vivomentioning

confidence: 93%

“…Some natural products have been found to protect against liver injuries [166][167][168][169][170]. Tea has also shown a beneficial effect on diet-and chemical-induced disorders in liver, including hepatic oxidative stress damage, inflammation, steatosis, and fibrosis [41,171,172].…”

Section: Hepato-protective Effectmentioning

confidence: 99%

Health Functions and Related Molecular Mechanisms of Tea Components: An Update Review

Tang

Meng

Gan

et al. 2019

IJMS

253

150

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Tea is widely consumed all over the world. Generally, tea is divided into six categories: White, green, yellow, oolong, black, and dark teas, based on the fermentation degree. Tea contains abundant phytochemicals, such as polyphenols, pigments, polysaccharides, alkaloids, free amino acids, and saponins. However, the bioavailability of tea phytochemicals is relatively low. Thus, some novel technologies like nanotechnology have been developed to improve the bioavailability of tea bioactive components and consequently enhance the bioactivity. So far, many studies have demonstrated that tea shows various health functions, such as antioxidant, anti-inflammatory, immuno-regulatory, anticancer, cardiovascular-protective, anti-diabetic, anti-obesity, and hepato-protective effects. Moreover, it is also considered that drinking tea is safe to humans, since reports about the severe adverse effects of tea consumption are rare. In order to provide a better understanding of tea and its health potential, this review summarizes and discusses recent literature on the bioactive components, bioavailability, health functions, and safety issues of tea, with special attention paid to the related molecular mechanisms of tea health functions.

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Evidence of similar protective effects afforded by white tea and its active component ‘EGCG’ on oxidative-stress mediated hepatic dysfunction during benzo(a)pyrene induced toxicity

Cited by 24 publications

References 53 publications

Benzo[a]pyrene induces pyroptotic and autophagic death through inhibiting PI3K/Akt signaling pathway in HL-7702 human normal liver cells

Benzo[a]pyrene induces pyroptotic and autophagic death through inhibiting PI3K/Akt signaling pathway in HL-7702 human normal liver cells

Isoorientin attenuates benzo[a]pyrene-induced liver injury by inhibiting autophagy and pyroptosis in vitro and vivo

Health Functions and Related Molecular Mechanisms of Tea Components: An Update Review

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