Verbena Attenuates Adriamycin-Induced Renal Tubular Injury via Inhibition of ROS-ERK1/2-NLRP3 Signal Pathway

Zhou, Yicen; Wu, Qijing; Du, Zhenfang; Huang, Min; Gao, Kun; Ma, Xiaowei; Zhang, Hui; Qiang, Sheng; Sun, Weijian

doi:10.1155/2022/7760945

Cited by 3 publications

(2 citation statements)

References 23 publications

(29 reference statements)

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“…[ 24 ] Earlier research shows that Dox results in renal tubular damage mediated by NLRP3 (NACHT, LRR, and PYD domain‐containing protein 3). [ 25 ] Agents with antioxidant and anti‐inflammatory properties may protect against Dox‐induced toxicity since oxidative stress and inflammatory response are important causes of Dox‐induced kidney impairment.…”

Section: Introductionmentioning

confidence: 99%

Betaine alleviates doxorubicin‐induced nephrotoxicity by preventing oxidative insults, inflammation, and fibrosis through the modulation of Nrf2/HO−1/NLRP3 and TGF‐β expression

Patel,

Yadav,

Singh

et al. 2023

J Biochem & Molecular Tox

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Doxorubicin (Dox) is an anthracycline antibiotic used to treat various cancers and shows severe toxicity in multiple organ systems, including kidneys. Evidence shows that betaine's antioxidant and anti‐inflammatory properties could prevent the onset of several disorders. Hence, the present study aims to investigate the therapeutic potential of betaine on Dox‐induced nephrotoxicity (DIN). Nephrotoxicity was induced in male Sprague Dawley rats using Dox at a dose of 4 mg/kg (cumulative dose: 20 mg/kg) by the intraperitoneal route and cotreated with betaine through oral gavage (200 and 400 mg/kg) for 28 days. At the end of the experiment, biochemical, oxidative stress parameters, histopathology, and qRT‐PCR were performed. DIN was indicated by elevated serum creatinine, urea, and decreased albumin levels representing kidney damage; the histopathological lesions (increased capsular space, renal tubule damage, and fibrosis) in renal tissues supported these biochemical findings. Interestingly, betaine treatment improves these alterations in Dox‐treated rats. Further, betaine treatment decreases the lipid peroxidation and nitrite concentration and increases the superoxide dismutases and catalase enzyme concentration in Dox‐treated rats. Fascinatingly, at the molecular level, DIN in rats shows upregulation of the Nrf2/HO‐1 gene, while betaine treatment attenuated its expression along with the downregulation of inflammatory genes (NLRP3, TLR‐4, TNF‐α, and IL‐6) and fibrosis‐related genes (TGF‐β and Acta2) expression in Dox‐treated rats. These results showed that betaine has reno‐protective properties by reducing inflammatory and fibrotic mediators and enhancing antioxidant capacity in the renal tissue of rats treated with Dox. We believe betaine can be exploited as a dietary supplement to attenuate DIN.

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Section: Introductionmentioning

confidence: 99%

Betaine alleviates doxorubicin‐induced nephrotoxicity by preventing oxidative insults, inflammation, and fibrosis through the modulation of Nrf2/HO−1/NLRP3 and TGF‐β expression

Patel,

Yadav,

Singh

et al. 2023

J Biochem & Molecular Tox

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“…Finally, renal tubular epithelial cell damage have a pivotal role in the development of chronic kidney disease too. Chronic renal failure also found as a worldwide public health issue; hence, agents which subsides the generation of reactive oxygen species could play a vital role in reducing adriamycin-induced renal tubular damage (11,12). Thereby further investigations of this aspect of adriamycin-adverse effects suggests.…”

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confidence: 99%

Keep the corners; adriamycin nephropathy

Momenzadeh

2022

J Nephropharmacol

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Paricalcitol prevents MAPK pathway activation and inflammation in adriamycin-induced kidney injury in rats

Deluque,

de Almeida,

Oliveira

et al. 2024

J Pathol Transl Med

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Background: Activation of the mitogen-activated protein kinase (MAPK) pathway induces uncontrolled cell proliferation in response to inflammatory stimuli. Adriamycin (ADR)-induced nephropathy (ADRN) in rats triggers MAPK activation and pro-inflammatory mechanisms by increasing cytokine secretion, similar to chronic kidney disease (CKD). Activation of the vitamin D receptor (VDR) plays a crucial role in suppressing the expression of inflammatory markers in the kidney and may contribute to reducing cellular proliferation. This study evaluated the effect of pre-treatment with paricalcitol on ADRN in renal inflammation mechanisms. Methods: Male Sprague-Dawley rats were implanted with an osmotic minipump containing activated vitamin D (paricalcitol, Zemplar, 6 ng/day) or vehicle (NaCl 0.9%). Two days after implantation, ADR (Fauldoxo, 3.5 mg/kg) or vehicle (NaCl 0.9%) was injected. The rats were divided into four experimental groups: control, n = 6; paricalcitol, n = 6; ADR, n = 7 and, ADR + paricalcitol, n = 7. Results: VDR activation was demonstrated by increased CYP24A1 in renal tissue. Paricalcitol prevented macrophage infiltration in the glomeruli, cortex, and outer medulla, prevented secretion of tumor necrosis factor-α, and interleukin-1β, increased arginase I and decreased arginase II tissue expressions, effects associated with attenuation of MAPK pathways, increased zonula occludens-1, and reduced cell proliferation associated with proliferating cell nuclear antigen expression. Paricalcitol treatment decreased the stromal cell-derived factor 1α/chemokine C-X-C receptor type 4/β-catenin pathway. Conclusions: Paricalcitol plays a renoprotective role by modulating renal inflammation and cell proliferation. These results highlight potential targets for treating CKD.

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Verbena Attenuates Adriamycin-Induced Renal Tubular Injury via Inhibition of ROS-ERK1/2-NLRP3 Signal Pathway

Cited by 3 publications

References 23 publications

Betaine alleviates doxorubicin‐induced nephrotoxicity by preventing oxidative insults, inflammation, and fibrosis through the modulation of Nrf2/HO−1/NLRP3 and TGF‐β expression

Betaine alleviates doxorubicin‐induced nephrotoxicity by preventing oxidative insults, inflammation, and fibrosis through the modulation of Nrf2/HO−1/NLRP3 and TGF‐β expression

Keep the corners; adriamycin nephropathy

Paricalcitol prevents MAPK pathway activation and inflammation in adriamycin-induced kidney injury in rats

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