Ameliorative effects of different doses of selenium against fluoride-triggered apoptosis and oxidative stress-mediated renal injury in rats through the activation of Nrf2/HO-1/NQO1 signaling pathway

Hu, Yingjun; Yan, Zipeng; He, Ya‐Ling; Li, Yan; Li, Meng; Li, Yuanyuan; Zhang, Dingli; Zhao, Yangfei; Ommati, Mohammad Mehdi; Wang, Jundong; Huo, Meijun; Wang, Jinming

doi:10.1016/j.fct.2023.113647

Cited by 9 publications

(3 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Here, our study depicted that Keap1 protein expression was increased and Nrf2, HO-1, and NQO1 protein levels were elevated in rats with CI-AKI, while these effects were prominently suppressed in CI-AKI rats with SS pretreatment, suggesting that SS activated Nrf2/ARE signaling transduction in the injured renal tissue. A recent study proposed that SS ameliorates fluoride-evoked oxidative renal injury in a rat model by activating Nrf2/HO-1/NQO1 signaling [ 31 ], which partially supports our results.…”

Section: Discussionsupporting

confidence: 90%

Sodium selenite attenuates inflammatory response and oxidative stress injury by regulating the Nrf2/ARE pathway in contrast-induced acute kidney injury in rats

Xiang,

Tan,

Zhang

et al. 2024

BMC Nephrol

View full text Add to dashboard Cite

Background Contrast-induced acute kidney injury (CI-AKI) is an acute renal complication that occurs after intravascular contrast agent administration. Sodium selenite (SS) is an inorganic source of Se and has potent antioxidant properties. This study intends to examine its anti-inflammatory and antioxidant effects in CI-AKI. Methods A rat CI-AKI model was established with the pretreatment of SS (0.35 mg/kg). Hematoxylin-eosin staining was employed for histopathological analysis of rat kidney specimens. Biochemical analysis was conducted for renal function detection. Tissue levels of oxidative stress-related markers were estimated. Reverse transcription-quantitative polymerase chain reaction revealed the mRNA levels of proinflammatory cytokines. Western blotting showed the Nrf2 signaling-related protein expression in the rat kidney. Results SS administration alleviated the renal pathological changes and reduced the serum levels of serum creatinine, blood urea nitrogen, neutrophil gelatinase-associated lipocalin, cystatin C, and urinary level of kidney injury molecule-1 in CI-AKI rats. SS attenuated oxidative stress and inflammatory response in CI-AKI rat kidney tissues. SS activated the Nrf2 signaling transduction in the renal tissues of rats with CI-AKI. Conclusion SS ameliorates CI-AKI in rats by reducing oxidative stress and inflammation via the Nrf2 signaling.

show abstract

Section: Discussionsupporting

confidence: 90%

Sodium selenite attenuates inflammatory response and oxidative stress injury by regulating the Nrf2/ARE pathway in contrast-induced acute kidney injury in rats

Xiang,

Tan,

Zhang

et al. 2024

BMC Nephrol

View full text Add to dashboard Cite

show abstract

“…Nrf2/HO-1/NQO1 pathway is vital for antioxidant stress response. Nrf2 is primary transcription factor for antioxidant stress response regulation, and HO-1 and NQO1 are primary downstream enzymes [ 42 , 43 ]. Currently, Nrf2 is considered to be an important negative regulator in the process of ferroptosis [ 44 ].…”

Section: Discussionmentioning

confidence: 99%

Orexin-A alleviates ferroptosis by activating the Nrf2/HO-1 signaling pathway in traumatic brain injury

Kang,

Ren,

Huang

et al. 2024

Aging

View full text Add to dashboard Cite

Background: Traumatic Brain Injury (TBI) has high disability and mortality rate. Oxidative stress and ferroptosis are important pathophysiological characteristics after TBI. Orexin-A (OXA) can alleviate neuronal damage in diverse neurological disorders. Nevertheless, the role and mechanism of OXA in TBI stay unknown. Objectives: The research investigated protection influence of OXA on TBI and its potential mechanisms. Methods: Male Sprague-Dawley rats were randomly grouped into: sham, TBI, TBI + normal saline (NS) and TBI+OXA groups. TBI model was constructed in rat via modified Feeney’s approach, and OXA treatment was administered following construction of TBI model. Results: Relative to TBI+NS group, TBI+OXA group displayed greatly recovered tissue damage and neurological deficits. Additionally, OXA eased oxidative stress as well as ferroptosis in cerebral cortex of rats following TBI. Furthermore, OXA increased Nrf2 expression and regulating factors HO-1 and NQO1 in cerebral cortex of TBI rats. Conclusions: Our research found OXA may restrain ferroptosis via Nrf2/HO-1 signaling pathway activation, thereby reducing brain injury after TBI.

show abstract

“…Malonic dialdehyde (MDA) is one of the most important products of membrane lipid peroxidation, and the production of MDA can also exacerbate cell damage. Therefore, MDA is a commonly used as an index to evaluate the oxidation stress 39 . The level of MDA (Figure 3E) showed fructose induce systemic oxidative stress which are similar with other previous study.…”

Section: Discussion/ Conclusionmentioning

confidence: 99%

Fructose aggravating colon barrier dysfunction by decreasing gut bacteria metabolites indole-3-carboxaldehyde and inhibiting activation of aryl hydrocarbon receptor in vivo and in vitro

Song,

Pang,

Peng

et al. 2024

Food Science and Human Wellness

View full text Add to dashboard Cite

Background: Fructose may induce non-alcoholic fatty acids (NAFLD) due to the gut-liver axis interactions. The mechanism of fructose impairing colon barrier is unrevealed.Methods: Normal and DSS-induced Sprague-Dawley rats fed by 35% fructose diets were used to evaluate colon barrier functions. Microbiome and metabolome were applied to screen potential biomarker bacteria and metabolites induced by fructose. HT-29 cells were applied to validate metabolite biomarker indoleacrylic acid (IAA) and indole-3-carboxaldehyde (I3A) function in colon barrier which impaired by fructose.Results: Fructose induced colon barrier dysfunction, aggravated colon impairment in DSS-induced rats. With fructose intake, the colon length shortened, goblet numbers declined, inflammation infiltration induced, inflammatory cytokines increased, and apoptosis signals upregulated in colon tissue. Moreover, fructose induced dysbiosis of microbiota and their metabolites. Adlercreutzia, Holdemania were screened out as potential bacteria biomarkers, IAA and I3A as tryptophan metabolites were selected as metabolite biomarkers inhibited by fructose. IAA and I3A treatment alleviated the impairment induced by fructose by increasing trans epithelial electric resistance (TEER) value, tight junction proteins (TJPs), and AhR activity in HT-29 cell.Conclusion: Fructose stimulated inflammation, apoptosis, gut bacteria alteration, and induced the reduction of IAA and I3A. Since fructose inhibited production of IAA and I3A, AhR remained inactivated and consequently induced colon barrier dysfunction.

show abstract

Ameliorative effects of different doses of selenium against fluoride-triggered apoptosis and oxidative stress-mediated renal injury in rats through the activation of Nrf2/HO-1/NQO1 signaling pathway

Cited by 9 publications

References 52 publications

Sodium selenite attenuates inflammatory response and oxidative stress injury by regulating the Nrf2/ARE pathway in contrast-induced acute kidney injury in rats

Sodium selenite attenuates inflammatory response and oxidative stress injury by regulating the Nrf2/ARE pathway in contrast-induced acute kidney injury in rats

Orexin-A alleviates ferroptosis by activating the Nrf2/HO-1 signaling pathway in traumatic brain injury

Fructose aggravating colon barrier dysfunction by decreasing gut bacteria metabolites indole-3-carboxaldehyde and inhibiting activation of aryl hydrocarbon receptor in vivo and in vitro

Contact Info

Product

Resources

About