Protective effect of Salidroside on hypoxia‐related liver oxidative stress and inflammation via Nrf2 and JAK2/STAT3 signaling pathways

Xiong, Yanlei; Wang, Yueming; Teng, Lianghong

doi:10.1002/fsn3.2459

Cited by 28 publications

(14 citation statements)

References 44 publications

(46 reference statements)

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“…Cytokines bind to receptors, resulting in receptor-coupled JAK aggregation and the activation of adjacent JAKs through mutual phosphorylation. The activated JAKs phosphorylate the tyrosine site on the receptor, causing the receptor to generate a STAT binding region and then phosphorylate STATs ( O'Shea et al, 2015 ; Johnson et al, 2018 ; Xiong et al, 2021 ). In a septic mouse model, blocking the JAK2/STAT3 signaling pathway significantly reduced the levels of HMGB1 and key cytokines and alleviated multi-organ injury ( Hui et al, 2009 ; Xin et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Intermedin Reduces Oxidative Stress and Apoptosis in Ventilator-Induced Lung Injury via JAK2/STAT3

Fan

Yang

et al. 2022

Front. Pharmacol.

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Mechanical ventilation is an effective treatment for acute respiratory distress syndrome (ARDS), which can improve the prognosis of ARDS to a certain extent. However, it may further aggravate lung tissue injury, which is defined as ventilator-induced lung injury (VILI). Intermedin (IMD) belongs to the calcitonin gene-related peptide (CPRP) superfamily. Our previous studies have found that IMD reduces the expression proinflammatory cytokines, down-regulates nuclear translocation and improves the integrity of endothelial barrier in ARDS. However, the effect of IMD on VILI has not been clarified. Oxidative stress imbalance and apoptosis are the main pathophysiological characteristics of VILI. In the current study, we used C57B6/J mice and human pulmonary microvascular endothelial cells (HPMECs) to establish a VILI model to analyze the effects of IMD on VILI and explore its potential mechanism. We found that IMD alleviated lung injury and inflammatory response in VILI, mainly in reducing ROS levels, upregulating SOD content, downregulating MDA content, reducing the expression of Bax and caspase-3, and increasing the expression of Bcl-2. In addition, we also found that IMD played its anti-oxidative stress and anti-apoptotic effects via JAK2/STAT3 signaling. Our study may provide some help for the prevention and treatment of VILI.

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Section: Discussionmentioning

confidence: 99%

Intermedin Reduces Oxidative Stress and Apoptosis in Ventilator-Induced Lung Injury via JAK2/STAT3

Fan

Yang

et al. 2022

Front. Pharmacol.

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“…Inflammatory cytokines play a crucial part in inflammatory reactions and tissue injuries or repairs [86–89] . Studies have indicated that SDS could obviously inhibit the expression of inflammatory cytokines in T2D, CCl 4 , furan, hypoxia, HFHC diet and HFD‐induced liver damage [36,90–93] . The NLRP3 inflammasome participates in the generation of mature IL‐1β and evokes inflammatory reaction.…”

Section: Protective Effect Of Sds On Nafld/nashmentioning

confidence: 99%

“…[86][87][88][89] Studies have indicated that SDS could obviously inhibit the expression of inflammatory cytokines in T2D, CCl 4 , furan, hypoxia, HFHC diet and HFD-induced liver damage. [36,[90][91][92][93] The NLRP3 inflammasome participates in the generation of mature IL-1β and evokes inflammatory reaction. Recently, NLRP3 inflammasome has been proven to perform a significant part in the development of NAFLD/NASH.…”

Section: Regulating Inflammationmentioning

confidence: 99%

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Salidroside in the Treatment of NAFLD/NASH

Liu

Liang

et al. 2022

Chemistry & Biodiversity

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Non‐alcoholic fatty liver disease (NAFLD) is the commonest reason for chronic liver diseases in the world and is commonly related to the hepatic manifestation of the metabolic syndrome. Non‐alcoholic steatohepatitis (NASH) is a deteriorating form of NAFLD, which can eventually develop into fibrosis, cirrhosis, and liver cancer. The reason for NAFLD/NASH development is complicated, such as liver lipid metabolism, oxidative stress, inflammatory response, apoptosis and autophagy, liver fibrosis and gut microbiota. Apart from bariatric surgery and lifestyle changes, officially approved drug therapy for NAFLD/NASH treatment is lacking. Salidroside (SDS) is a phenolic compound extensively distributed in the tubers of Rhodiola plants, which possesses many significant biological activities. This review summarized the related targets regulated by SDS in treating NAFLD/NASH. It is indicated that SDS could improve the status of NAFLD/NASH by ameliorating abnormal lipid metabolism, inhibiting oxidative stress, regulating apoptosis and autophagy, reducing inflammatory response, alleviating fibrosis and regulating gut microbiota. In conclusion, although the multiple bioactivities of SDS have been confirmed, the clinical data are inadequate and need to become the focus of attention in the later study.

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“…However, whether this improvement can be extended under IR conditions and its underlying mechanism remains unclear. Recently, Rhodiola was found to be a Nuclear factor erythroid 2-related factor 2 (Nrf2) activator, which enhances the antioxidant system to exert neuroprotective effects 19 or relieve hypoxia-induced liver injury 20 . Thus, we hypothesize that Rhodiola activates Nrf2 and the downstream antioxidant system to regulate mitochondrial dynamic homeostasis, finally strengthening cardiac anti-stress capacity under IR conditions.…”

Section: Introductionmentioning

confidence: 99%

Rhodiola pre-conditioning reduces exhaustive exercise-induced myocardial injury of insulin resistant mice

You

Cheng

Dun

et al. 2022

Sci Rep

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Myocardial injury reduction and recovery under acute cardiac stress are adversely impacted by insulin resistance (IR). We previously demonstrated that Rhodiola improved cardiac anti-stress capacity in mice. Thus, this study focuses on the preventive efficacy of Rhodiola on exhaustive exercise (EE)-induced myocardial injury of IR mice. An 8-week high-fat diet (HFD) model of IR mice was established. Rhodiola was administrated by garaging. After the 8-week intervention, half of the mice performed EE to simulate acute cardiac stress, and determine myocardial injury; The remaining mice were sacrificed following fasting to assess metabolic disorder. We found myocardial injury induced by EE in IR mice was worse and was alleviated by Rhodiola pre-conditioning. Further, the nuclear factor erythroid 2-related factor 2 (Nrf2)-related antioxidant system was impaired by HFD, while mitochondrial dynamic fusion and fission were activated by HFD as a physiological protective compensation. The Rhodiola administration rescued Nrf2 impairment and further facilitated mitochondrial fusion and fission. All these results indicate that Rhodiola is a potential treatment for the prevention of cardiac events in type 2 diabetes mellitus and metabolic syndrome patients, and the Nrf2-related antioxidant activity and mitochondrial dynamics are the proposed mechanisms.

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Protective effect of Salidroside on hypoxia‐related liver oxidative stress and inflammation via Nrf2 and JAK2/STAT3 signaling pathways

Cited by 28 publications

References 44 publications

Intermedin Reduces Oxidative Stress and Apoptosis in Ventilator-Induced Lung Injury via JAK2/STAT3

Intermedin Reduces Oxidative Stress and Apoptosis in Ventilator-Induced Lung Injury via JAK2/STAT3

Salidroside in the Treatment of NAFLD/NASH

Rhodiola pre-conditioning reduces exhaustive exercise-induced myocardial injury of insulin resistant mice

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