Effects of quercetin and menadione on intestinal calcium absorption and the underlying mechanisms

Marchionatti, Ana Maria Estivalete; Pacciaroni, Adriana; Talamoni, Nori G. Tolosa de

doi:10.1016/j.cbpa.2012.09.007

Cited by 22 publications

(16 citation statements)

References 45 publications

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“…Natsume et al [26] reported that quercetin suppressed the ER stress caused by calcium dynamics dysregulation by the inhibition of PI3K. Quercetin may be useful in preventing inhibition of intestinal Ca 2+ absorption caused by menadione or other substances that deplete glutathione leading to oxidative stress and apoptosis [27]. Quercetin may protect the GI mucosa against the adverse effects of NSAIDs by preventing mitochondrial dysfunction and by regulating intracellular Ca 2+ homeostasis [6].…”

Section: Discussionmentioning

confidence: 99%

Changes of intracellular Ca<sup>2+</sup> in quercetin-induced autophagy progression

Cui

Luo

et al. 2015

ABBS

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Quercetin was previously reported to exhibit significant anti-proliferative activities, and its major effect on tumors was to induce cell apoptosis or autophagy. However, the specific mechanism remains controversial. In this study, autophagy induced by quercetin was determined with various methods. Intracellular Ca 2+ ([Ca 2+ ] i ) was measured after being incubated with Fluo-3 acetoxymethyl (AM). At the same time, the relationship between the intracellular Ca 2+ and autophagy induced by quercetin was further analyzed. These results showed that autophagy induced by quercetin (0-50 µg/ml) in HepG2 cells was in a dose-dependent manner. Meanwhile, when autophagy was induced by quercetin, [Ca 2+ ] i was significantly increased. And after being incubated with calcium chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N-tetraacetic acid-AM, autophagy was suppressed, which implied that [Ca 2+ ] i elevation appeared to be the cause for autophagy induction. These results suggested that calcium from intracellular calcium storage may play an important role in quercetininduced autophagy.

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Section: Discussionmentioning

confidence: 99%

Changes of intracellular Ca<sup>2+</sup> in quercetin-induced autophagy progression

Cui

Luo

et al. 2015

ABBS

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“…This means that the majority of mitochondria remained competent for ATP synthesis, making possible the process of apoptosis[91] and a poor intestinal Ca 2+ absorption. MEN not only produced intestinal apoptosis through the mitochondrial pathway, but also by triggering the expression of FAS/FASL/caspase-3[92]. Although an enhancement in the Cu 2+ /Zn 2+ -SOD, CAT, GPx and Mn 2+ -SOD activities could represent cytoprotective mechanisms against the oxidant effects, they were insufficient to avoid an inhibition in the overall process of intestinal Ca 2+ absorption[92-94].…”

Section: Actions Of Pro-oxidants On Intestinal Calcium Absorptionmentioning

confidence: 99%

“…MEN not only produced intestinal apoptosis through the mitochondrial pathway, but also by triggering the expression of FAS/FASL/caspase-3[92]. Although an enhancement in the Cu 2+ /Zn 2+ -SOD, CAT, GPx and Mn 2+ -SOD activities could represent cytoprotective mechanisms against the oxidant effects, they were insufficient to avoid an inhibition in the overall process of intestinal Ca 2+ absorption[92-94]. The results supported previous data showing alterations in the intracellular thiols and Ca 2+ homeostasis, ATP depletion and DNA breakage after toxic MEN concentrations[95-97].…”

Section: Actions Of Pro-oxidants On Intestinal Calcium Absorptionmentioning

confidence: 99%

“…It has been suggested that natural or synthetic compounds would help to overcome the disequilibrium[103,104]. In our laboratory, we have demonstrated that the inhibition of intestinal Ca 2+ absorption caused by oxidants, mainly causing GSH depletion, could be either prevented or restored by quercetin[92] (QT, a plant derived flavonoid), melatonin[90,94] (MEL, a natural antioxidant present in humans), lithocholic (LCA)[105] or ursodeoxycholic (UDCA)[106] acids (bile acids less hydrophobic than deoxycholic acid). QT is a polyphenolic flavonoid found in several fruits and vegetables of the human diet[107], mainly highly concentrated in onions, tea and apples[108].…”

Section: Antioxidants and Their Molecular Mechanisms For The Preservamentioning

confidence: 99%

“…Similarly, QT abolishes the GSH depletion caused by the quinone, but QT alone does not modify the intestinal GSH content. The flavonoid also avoids changes in the mitochondrial membrane permeability and abrogates the activation of FASL/FAS/caspase-3 pathway caused by MEN[92]. Conclusively, QT may be useful to prevent the inhibition of intestinal Ca 2+ absorption caused by MEN or other GSH depleting drugs by blocking the oxidative stress and apoptosis.…”

Section: Antioxidants and Their Molecular Mechanisms For The Preservamentioning

confidence: 99%

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Oxidative stress, antioxidants and intestinal calcium absorption

Barboza¹,

Guizzardi²,

Moine³

et al. 2017

WJG

106

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The disequilibrium between the production of reactive oxygen (ROS) and nitrogen (RNS) species and their elimination by protective mechanisms leads to oxidative stress. Mitochondria are the main source of ROS as by-products of electron transport chain. Most of the time the intestine responds adequately against the oxidative stress, but with aging or under conditions that exacerbate the ROS and/or RNS production, the defenses are not enough and contribute to developing intestinal pathologies. The endogenous antioxidant defense system in gut includes glutathione (GSH) and GSH-dependent enzymes as major components. When the ROS and/or RNS production is exacerbated, oxidative stress occurs and the intestinal Ca2+ absorption is inhibited. GSH depleting drugs such as DL-buthionine-S,R-sulfoximine, menadione and sodium deoxycholate inhibit the Ca2+ transport from lumen to blood by alteration in the protein expression and/or activity of molecules involved in the Ca2+ transcellular and paracellular pathways through mechanisms of oxidative stress, apoptosis and/or autophagy. Quercetin, melatonin, lithocholic and ursodeoxycholic acids block the effect of those drugs in experimental animals by their antioxidant, anti-apoptotic and/or anti-autophagic properties. Therefore, they may become drugs of choice for treatment of deteriorated intestinal Ca2+ absorption under oxidant conditions such as aging, diabetes, gut inflammation and other intestinal disorders.

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Lipopolysaccharide‐induced expression of FAS ligand in cultured immature boar sertoli cells through the regulation of pro‐inflammatory cytokines and miR‐187

Wang

Zhang

Yang

et al. 2015

Molecular Reproduction Devel

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Lipopolysaccharide (LPS) induces germ cell apoptosis, but its mechanism of action is not clear. One possibility is that LPS regulates the expression of FAS ligand (FASLG) in Sertoli cells, which will then influence germ cell apoptosis. In this study, LPS reduced the viability of cultured, immature boar Sertoli cells in a time- and dose-dependent manner; enhanced the production of pro-inflammatory cytokines including tumor necrosis factor α (TNFA), interleukin-1β (IL1B), nitric oxide (NO), and transforming growth factor-β (TGFB); and increased the expression of FASLG in a dose-dependent manner. While 10 μg/ml LPS enhanced the expression of FASLG, reduced cell cycle progression, and impaired the ultrastructure of Sertoli cells, this dose did not induce apoptosis. LPS also had no effect on the activity or expression of matrix metalloproteinases 2 or 9 (MMP2 or MMP9). In contrast, the expression of ssc-miR-187 increased following LPS challenge, and inhibition of ssc-miR-187 blocked LPS-induced expression of FASLG. Our results therefore suggest that LPS reduces the viability of and enhances FASLG expression in cultured, immature boar Sertoli cells through elevated secretion of TNFA, IL1B, NO, and TGFB as well as through the regulation of ssc-miR-187 potency.

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Effects of quercetin and menadione on intestinal calcium absorption and the underlying mechanisms

Cited by 22 publications

References 45 publications

Changes of intracellular Ca<sup>2+</sup> in quercetin-induced autophagy progression

Changes of intracellular Ca<sup>2+</sup> in quercetin-induced autophagy progression

Oxidative stress, antioxidants and intestinal calcium absorption

Lipopolysaccharide‐induced expression of FAS ligand in cultured immature boar sertoli cells through the regulation of pro‐inflammatory cytokines and miR‐187

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Effects of quercetin and menadione on intestinal calcium absorption and the underlying mechanisms

Cited by 22 publications

References 45 publications

Changes of intracellular Ca&lt;sup&gt;2+&lt;/sup&gt; in quercetin-induced autophagy progression

Changes of intracellular Ca&lt;sup&gt;2+&lt;/sup&gt; in quercetin-induced autophagy progression

Oxidative stress, antioxidants and intestinal calcium absorption

Lipopolysaccharide‐induced expression of FAS ligand in cultured immature boar sertoli cells through the regulation of pro‐inflammatory cytokines and miR‐187

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Changes of intracellular Ca<sup>2+</sup> in quercetin-induced autophagy progression

Changes of intracellular Ca<sup>2+</sup> in quercetin-induced autophagy progression