Protective Effect of Nebivolol against Oxidative Stress Induced by Aristolochic Acids in Endothelial Cells

Antoine, Marie-Hélène; Husson, Cécile; Yankep, Tatiana; Mahria, Souhaila; Tagliatti, Vanessa; Colet, Jean‐Marie; Nortier, Joëlle

doi:10.3390/toxins14020132

Cited by 3 publications

(2 citation statements)

References 50 publications

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“…Dietary thiamine supplementation increases the expression of Nrf2 and its downstream proteins and decreases the phosphorylation of NF-κB in goat rumen epithelial cells (Ma et al, 2021). Glycerophosphocholine is a lipid metabolite exported from cells expressing high levels of Nrf2 and is thought to prevent oxidative stress-induced cell damage (Saigusa et al, 2020;Antoine et al, 2022). L-Glutamine can inhibit the activation of NF-κB (Kim and Kim, 2017), whereas indoxyl sulfate, accumulating in the sera of mice with colon cancer, enhances the expression of proinflammatory cytokines (Li et al, 2015).…”

Section: Hxzq Regulates Nrf2/nf-κb Signalingmentioning

confidence: 99%

Huoxiang Zhengqi alleviates azoxymethane/dextran sulfate sodium-induced colitis-associated cancer by regulating Nrf2/NF-κB/NLRP3 signaling

Dong

Liu²,

Cao³

et al. 2022

Front. Pharmacol.

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Colitis-associated cancer (CAC) is a subtype of inflammatory bowel disease (IBD)-associated colorectal cancer. Huoxiang Zhengqi (HXZQ) is a classical Chinese herbal medicine and has been used to treat intestinal disorders, however, anti-CAC effects and underlying mechanisms of HXZQ have not been reported. An azoxymethane/dextran sulfate sodium-induced CAC mice model was used to investigate the anti-CAC effect of HXZQ. HXZQ significantly reduced colonic inflammation, suppressed the size and number of tumors, and reduced the levels of pro-inflammatory cytokines (interleukin [IL]-1α, IL-1β, IL-6, IL-17A, IL-21, IL-23, granulocyte macrophage-colony stimulating factor, and tumor necrosis factor-α) and oxidative stress markers (reactive oxygen species and malondialdehyde), and increased the levels of anti-inflammatory cytokines (IL-10 and IL-27) in CAC mice. Intestinal microbiota and serum metabolomics analyses indicated that HXZQ altered the gut microbial composition and the abundance of 29 serum metabolites in CAC mice. Additionally, HXZQ activated the nuclear factor-erythroid factor 2-related factor 2 (Nrf2) signaling pathway and increased the levels of antioxidants such as catalase (CAT), heme oxygenase-1 (HO-1), NAD(P)H quinone oxidoreductases-1 (NQO-1), and superoxide dismutase-1 (SOD-1). HXZQ inhibited the activation of the nuclear factor kappa-B (NF-κB) signaling pathway and decreased the expression of NLR family pyrin domain containing 3 (NLRP3) by inhibiting the phosphorylation of inhibitor of nuclear factor kappa-B (IκB), inhibitor of nuclear factor kappa-B kinase (IKK), and NF-κB. In conclusion, HXZQ alleviated CAC in mice by modulating the intestinal microbiota and metabolism, activating Nrf2-mediated antioxidant response, and inhibiting NF-κB-mediated NLRP3 inflammasome activation against inflammation. The present data provide a reference for the use of HXZQ as a therapeutic or combination agent for clinical CAC treatment.

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Section: Hxzq Regulates Nrf2/nf-κb Signalingmentioning

confidence: 99%

Huoxiang Zhengqi alleviates azoxymethane/dextran sulfate sodium-induced colitis-associated cancer by regulating Nrf2/NF-κB/NLRP3 signaling

Dong

Liu²,

Cao³

et al. 2022

Front. Pharmacol.

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“…indicating that CAT has a therapeutic effect ANN. Oxidative stress was considered as the main pathogenesis of AAN(Antoine et al 2022;Zhang, ShiYang, et al 2019;Liu et al 2020). Therefore, we explored the protective mechanism of CAT on tubular epithelial cells based on the Nrf2/HO-1 antioxidant system.…”

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confidence: 99%

Catalpol attenuates renal injury by regulating oxidative stress and inflammation response

Liu

Wang

Zhou

et al. 2022

Preprint

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Background: Aristolochic acid I (AA-I) can damage the structure and function of kidney, but there are few prevention strategies at present. In this study, we investigated the protective effects and mechanism of Rehmannia glutinosa extract-catalpol (CAT) on renal injury caused by AA-I. Methods: In vitro, NRK-52E cells were administered with AA-I (40 μM) or/and CAT (10 μM, 5 μM) for 24 h. In vivo, C57BL/6NJ male mice were administered with AA-I (10 mg/kg) or/and CAT (100 mg/kg, 10 mg/kg) for 28 d. Clinical symptoms, histopathology, Elisa, quantitative RT-PCR, Westernblot, immunocytochemistry, immunofluorescence and flow cytometry were used to evaluate the protective effect of CAT on renal injury. Results: In the model group, the body weight and renal function of mice decreased significantly, and the pathological damage of renal tissue was obvious. Compared with the model group, CAT can significantly improve the kidney structure and function. Activate NF-E2-related-factor-2 (Nrf2) signal pathway, increase antioxidant enzyme activity and decrease ROS and MDA levels. CAT can also inhibit the nuclear-factor-kappa-B (NF-κB) signaling pathway and reduce the expression of Cyt-c, TNF-α and pro-IL-1β. In addition, CAT can reduce Ca2+ concentration, endoplasmic reticulum (ER) stress and mitochondrial damage, thus reducing mitochondrial pathway apoptosis and cell apoptosis rate. And both Nrf2 and NF-κB are the main targets of CAT in alleviating AA-I-induced renal injury. Conclusion: CAT can attenuate the damage of renal structure and function through Nrf2/NF-κB pathways. CAT can inhibit inflammation and oxidative stress, further reducing the mitochondrial pathway apoptosis and endoplasmic reticulum stress pathway apoptosis.

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Catalpol from Rehmannia glutinosa Targets Nrf2/NF-κB Signaling Pathway to Improve Renal Anemia and Fibrosis

Liu,

Xu,

Wang

et al. 2024

Am. J. Chin. Med.

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Rehmannia glutinosa is widely recognized as a prominent medicinal herb employed by practitioners across various generations for the purpose of fortifying kidney yin. Within Rehmannia glutinosa, the compound known as catalpol (CAT) holds significant importance as a bioactive constituent. However, the protective effects of CAT on kidneys, including ameliorative effects on chronic kidney disease — most prominently renal anemia and renal fibrosis — have not been clearly defined. In this study, the kidney injury model of NRK-52E cells and C57BL/6N male mice was prepared by exposure to aristolochic acid I (AA-I), and it was discovered that CAT could ameliorate oxidative stress injury, inflammatory injury, apoptosis, renal anemia, renal fibrosis, and other renal injuries both in vivo and in vitro. Further treatment of NRK-52E cells with Nrf2 inhibitors (ML385) and activators (ML334), as well as NF-[Formula: see text]B inhibitors (PDTC), validated CAT’s ability to target Nrf2 activation. Furthermore, the expression of phosphorylated NF-[Formula: see text]B p65, IL-6, and Cleaved-Caspase3 protein was inhibited. CAT also inhibited NF-[Formula: see text]B, and then inhibited the expression of IL-6, p-STAS3, TGF-[Formula: see text]1 protein. Therefore, CAT can regulate Nrf2/NF-[Formula: see text]B signaling pathway, significantly correct renal anemia and renal fibrosis, and is conducive to the preservation of renal structure and function, thus achieving a protective effect on the kidneys.

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Protective Effect of Nebivolol against Oxidative Stress Induced by Aristolochic Acids in Endothelial Cells

Cited by 3 publications

References 50 publications

Huoxiang Zhengqi alleviates azoxymethane/dextran sulfate sodium-induced colitis-associated cancer by regulating Nrf2/NF-κB/NLRP3 signaling

Huoxiang Zhengqi alleviates azoxymethane/dextran sulfate sodium-induced colitis-associated cancer by regulating Nrf2/NF-κB/NLRP3 signaling

Catalpol attenuates renal injury by regulating oxidative stress and inflammation response

Catalpol from Rehmannia glutinosa Targets Nrf2/NF-κB Signaling Pathway to Improve Renal Anemia and Fibrosis

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