Sulforaphane prevents chromium-induced lung injury in rats via activation of the Akt/GSK-3β/Fyn pathway

Lv, Yueying; Jiang, Huijie; Li, Siyu; Han, Bing; Liu, Yan; Yang, Daqian; Li, Jiayi; Yang, Qingyue; Wu, Pengfei; Zhang, Zhigang

doi:10.1016/j.envpol.2019.113812

Cited by 76 publications

(33 citation statements)

References 72 publications

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“…SOD is a free radical scavenging factor in vivo and its activity reflects the ability of cells to scavenge free radicals and resist lipid peroxidation. SOD plays a key role in preventing the formation of peroxides, anti-oxidative stress injury and anti-renal tubular injury (29). The present study also identified the augmenting effect of Trx on SOD in AKI mice.…”

Section: Discussionsupporting

confidence: 68%

Thioredoxin relieves lipopolysaccharide‑induced acute kidney injury in mice by reducing inflammation, oxidative stress and apoptosis

Wang

Zhang

Lu³

2021

Exp Ther Med

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Acute kidney injury (AKI) is a serious disease with rapid onset and a high mortality rate. It is therefore particularly important to identify a suitable method for treating AKI. Thioredoxin (Trx) is a potent anti-inflammatory and anti-oxidant protein that is prevalent in living organisms. The aim of the present study was to facilitate the clinical treatment of AKI via the study of Trx. Lipopolysaccharide (LPS) was used to construct an AKI model in mice and the mice were pre-treated with Trx to examine its effect on AKI. In addition, human renal tubular epithelial HK-2 cells were cultured and stimulated with Trx to examine its effect on inflammation, levels of oxidative stress and apoptosis in the HK-2 cells. The NF-κB signaling pathway is a classical inflammation-related pathway and the mechanism of Trx was investigated by evaluating the association between Trx and the NF-κB signaling pathway. Trx treatment reduced LPS-induced levels of inflammation, oxidative stress and apoptosis in the HK-2 cells. The activity of NF-κB signaling pathway was increased in LPS-induced HK-2 cells, while Trx treatment effectively reduced NF-κB signaling pathway activity. In addition, Trx treatment significantly reduced LPS-induced mouse AKI in vivo, which was characterized by a decrease in inflammatory factors in mouse serum, a decrease in AKI-associated molecules in mouse urine and a decrease in oxidative stress levels in mouse kidney tissue samples. Trx treatment reduced inflammation, levels of oxidative stress and apoptosis in HK-2 cells by inhibiting the NF-κB signaling pathway, thereby alleviating LPS-induced mouse AKI.

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Section: Discussionsupporting

confidence: 68%

Thioredoxin relieves lipopolysaccharide‑induced acute kidney injury in mice by reducing inflammation, oxidative stress and apoptosis

Wang

Zhang

Lu³

2021

Exp Ther Med

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“…Sulforaphane 153 is a natural compound in many green vegetables, possessing anti-inflammatory and anti-oxidative activities. Sulforaphane significantly prevented pulmonary damage induced by LPS through activating the Nrf2-ARE signaling pathway [ 407 ], protected against inhaled arsenic-induced ALI through activating the Nrf2-defense responses [ 408 ], ameliorated hyperoxia-induced ALI through regulating HMGB1 activity [ 409 ] as well as prevented chromium-induced pulmonary toxicity in rats through regulating the Nrf2-mediated Akt/GSK-3β/Fyn signaling pathway [ 410 ]. Moreover, sulforaphane also inhibited lung injury induced by oleic acid in rabbits through up-regulating the Nrf2 signaling pathway [ 411 ].…”

Section: Natural Compounds That Exert Anti-ali Effectsmentioning

confidence: 99%

Natural product derived phytochemicals in managing acute lung injury by multiple mechanisms

Zhou

et al. 2021

Pharmacological Research

193

108

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“…Therefore, exploration of more alternative treatments for IC is necessary. Nrf2 pathway has been proven to inhibit oxidative stress damage in cardiac myocyte damage [ 16 ], lung injury [ 17 , 18 ], and liver damage [ 19 , 20 ]. Increasing studies have shown that oxidative stress participates in IC [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

Nrf2 Pathway Ameliorates Bladder Dysfunction in Cyclophosphamide-Induced Cystitis via Suppression of Oxidative Stress

Chen

Shu

et al. 2021

Oxidative Medicine and Cellular Longevity

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Objective. To investigate the protective effect and molecular mechanism of nuclear factor E2-related factor 2 (Nrf2) pathway in interstitial cystitis (IC). Methods. We established a mouse model of IC by cyclophosphamide (CYP) in wild-type mice and Nrf2 gene knockout mice. We examined the histological and functional alterations, the changes of oxidative stress markers, and the expression of the antioxidant genes downstream of Nrf2 pathway. Results. After CYP administration, the mice showed urinary frequency and urgency, pain sensitization, decreased contractility, bladder edema, and oxidative stress disorder. Notably, the Nrf2-/- CYP mice had more severe symptoms. The mRNA and protein levels of antioxidant genes downstream of Nrf2 pathway were significantly upregulated in the Nrf2+/+ CYP mice, while there were no significant changes in the Nrf2-/- CYP mice. Conclusion. Nrf2 pathway protects bladder injury and ameliorates bladder dysfunction in IC, possibly by upregulating antioxidant genes and inhibiting oxidative stress.

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Sulforaphane prevents chromium-induced lung injury in rats via activation of the Akt/GSK-3β/Fyn pathway

Cited by 76 publications

References 72 publications

Thioredoxin relieves lipopolysaccharide‑induced acute kidney injury in mice by reducing inflammation, oxidative stress and apoptosis

Thioredoxin relieves lipopolysaccharide‑induced acute kidney injury in mice by reducing inflammation, oxidative stress and apoptosis

Natural product derived phytochemicals in managing acute lung injury by multiple mechanisms

Nrf2 Pathway Ameliorates Bladder Dysfunction in Cyclophosphamide-Induced Cystitis via Suppression of Oxidative Stress

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