Caffeine prevents oxalate-induced epithelial-mesenchymal transition of renal tubular cells by its anti-oxidative property through activation of Nrf2 signaling and suppression of Snail1 transcription factor

Kanlaya, Rattiyaporn; Subkod, Chonnicha; Nanthawuttiphan, Supanan; Thongboonkerd, Visith

doi:10.1016/j.biopha.2021.111870

Cited by 17 publications

(6 citation statements)

References 58 publications

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“…The role of Nrf2 in EMT has raised researchers’ interest in the past years but studies demonstrate contradictory results. Some studies have demonstrated that Nrf2 activation is associated with EMT induction [ 21 , 45 , 46 ] while others, as our results suggest, demonstrate that Nrf2 impairment leads to the induction of the EMT program [ 47 , 48 , 49 ] or, in the same way, that Nrf2 activation is associated with EMT inhibition [ 50 , 51 , 52 ]. Interestingly, it has also been described that Nrf2 may act as a phenotypic stability factor in restricting complete EMT by maintaining the cells in a hybrid epithelial/mesenchymal state [ 23 , 53 ].…”

Section: Discussionsupporting

confidence: 68%

Nrf2 Downregulation Contributes to Epithelial-to-Mesenchymal Transition in Helicobacter pylori-Infected Cells

Bacon

Seeneevassen

Fratacci

et al. 2022

Cancers

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Background: Gastric cancer, the fifth most common cancer worldwide, is mainly linked to Helicobacter pylori infection. H. pylori induces chronic inflammation of the gastric mucosa associated with high oxidative stress. Our study aimed at assessing the implication of Nrf2, a major regulator of cellular redox homeostasis, in H. pylori-induced gastric carcinogenesis. Methods: Using three different gastric epithelial cell lines, a non-cancerous (HFE-145) and two different subtypes of gastric cancer (AGS and MKN74), we analyzed the modulation of Nrf2 expression over time. After invalidation of Nrf2 by CRISPR-cas9, we assessed its role in H. pylori-induced epithelial-to-mesenchymal transition (EMT). Finally, we evaluated the expression of Nrf2 and ZEB1, a central EMT transcription factor, in human gastric tissues. Results: We first demonstrated that the Nrf2 signaling pathway is differentially regulated depending on the infection stage. Rapidly and transiently activated, Nrf2 was downregulated 24 h post-infection in a VacA-dependent manner. We then demonstrated that Nrf2 invalidation leads to increased EMT, which is even exacerbated after H. pylori infection. Finally, Nrf2 expression tended to decrease in human patients’ gastric mucosa infected with H. pylori. Conclusions: Our work supports the hypothesis that Nrf2 downregulation upon H. pylori infection participates in EMT, one of the most important events in gastric carcinogenesis.

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Section: Discussionsupporting

confidence: 68%

Nrf2 Downregulation Contributes to Epithelial-to-Mesenchymal Transition in Helicobacter pylori-Infected Cells

Bacon

Seeneevassen

Fratacci

et al. 2022

Cancers

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“…Concerning caffeine levels in the liver, it is known that almost all ingested caffeine reaches the liver, where it is metabolized (Nehlig 2018). Additionally, caffeine protects renal tubular cells by its antioxidative properties through activation of the Nrf2-signaling pathway (Kanlaya et al 2021). Therefore, under our conditions, caffeine likely has a direct effect on hepatic Nrf2, although more experiments are required to confirm the direct activation of the Nrf2-signaling pathway by caffeine.…”

Section: Caffeine May Decrease Liver Damage Bymentioning

confidence: 80%

The antioxidant and anti-inflammatory activities of caffeine effectively attenuate nonalcoholic steatohepatitis and thioacetamide-induced hepatic injury in male rats

Vargas-Pozada

Ramos‐Tovar²,

Acero-Hernández

et al. 2023

Can. J. Physiol. Pharmacol.

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The antioxidant effect of caffeine, associated with its ability to upregulate the nuclear factor-E2-related factor-2 (Nrf2)-signaling pathway, was explored as a possible mechanism for the attenuation of liver damage. Nonalcoholic steatohepatitis (NASH) was induced in rats by the administration of a high-fat, high-sucrose, high-cholesterol diet (HFSCD) for 15 weeks. Liver damage was induced in rats by intraperitoneal administration of thioacetamide (TAA) for six weeks. Caffeine was administered orally at a daily dose of 50 mg/kg body weight during the period of NASH induction to evaluate its ability to prevent disease development. Meanwhile, rats received TAA for three weeks, after which 50 mg/kg caffeine was administered daily for three weeks with TAA to evaluate its capacity to interfere with the progression of hepatic injury. HFSCD administration induced hepatic steatosis, decreased Nrf2 levels, increased oxidative stress, induced the activation of nuclear factor-κB (NF-κB), and elevated proinflammatory cytokine levels, leading to hepatic damage. TAA administration produced similar effects, excluding steatosis. Caffeine increased Nrf2 levels; attenuated oxidative stress markers, including malondialdehyde and 4-hydroxynonenal; restored normal, reduced glutathione levels; and reduced NF-κB activation, inflammatory cytokine levels, and damage. Our findings suggest that caffeine may be useful in the treatment of human liver diseases.

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“…Results of software simulation indicated that TF may influence the wound healing process through its ability to interact with Nrf2, thereby promoting its nuclear translocation. Since Nrf2 is an important transcription factor in the redox reaction system ( Kanlaya et al, 2021 ), we explored the potential role of Nrf2 played in TF-induced the cellular protective effect in HUVECs exposed to TBHP-induced oxidative stress. In order to determine whether TF promoted nuclear translocation of Nrf2 in the HUVECs, we carried out immunofluorescence staining on Nrf2, which suggested that TF induced the nuclear translocation of Nrf2 in the HUVECs ( Figure 4B ).…”

Section: Resultsmentioning

confidence: 99%

Theaflavin Attenuates TBHP-Induced Endothelial Cells Oxidative Stress by Activating PI3K/AKT/Nrf2 and Accelerates Wound Healing in Rats

Chen

et al. 2022

Front. Bioeng. Biotechnol.

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The treatment of wounds remains a clinical challenge because of poor angiogenesis under the wound bed, and increasingly, the patients’ need for functional and aesthetically pleasing scars. Previous reports have shown that Theaflavin can induce angiogenesis and terminate the progression of ischemic cardiovascular disease, but limited therapy is available for the management of cutaneous wounds. In this study, our in vitro work discovered that human umbilical vein endothelial cells (HUVECs) exposed to Theaflavin can alleviate apoptosis and cell dysfunction induced by tert-butyl hydroperoxide (TBHP). The cellular activity of HUVECs were assessed by cell tube formation, migration and adhesion. Mechanistically, Theaflavin protected HUVECs from TBHP-stimulated cell apoptosis through the activation of the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT)/nuclear factor (erythroid-derived 2)-like 2 (Nrf2) axis, so Nrf2 silencing can partly eliminate the cytoprotective effect of Theaflavin treatment. In in vivo experiments, administering Theaflavin orally can enhance vascularization in regenerated tissues and accelerate wound healing. In summary, our data served as a novel evidence for the wound healing treatment with Theaflavin, and certified the potential mechanism of Theaflavin, which can be used as a potential agent for cutaneous wound therapy.

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Caffeine prevents oxalate-induced epithelial-mesenchymal transition of renal tubular cells by its anti-oxidative property through activation of Nrf2 signaling and suppression of Snail1 transcription factor

Cited by 17 publications

References 58 publications

Nrf2 Downregulation Contributes to Epithelial-to-Mesenchymal Transition in Helicobacter pylori-Infected Cells

Nrf2 Downregulation Contributes to Epithelial-to-Mesenchymal Transition in Helicobacter pylori-Infected Cells

The antioxidant and anti-inflammatory activities of caffeine effectively attenuate nonalcoholic steatohepatitis and thioacetamide-induced hepatic injury in male rats

Theaflavin Attenuates TBHP-Induced Endothelial Cells Oxidative Stress by Activating PI3K/AKT/Nrf2 and Accelerates Wound Healing in Rats

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