Salidroside Attenuates Ventilation Induced Lung Injury via SIRT1-Dependent Inhibition of NLRP3 Inflammasome

Wang, Yan; Xu, Chang; Liu, Yujian; Mao, Yanfei; Zhou, Lv; Li, Si-Yuan; Zhu, Xiaoyan; Jiang, Lai

doi:10.1159/000477112

Cited by 44 publications

(36 citation statements)

References 57 publications

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“…In addition, SIRT1 is closely related to the activation of NLRP3 inflammasome . In rat cerebral ischaemia/reperfusion models and ventilation‐induced lung injury models, SIRT1‐dependent inhibition of NLRP3 inflammatory body activation . Therefore, it may be assumed that quercetin effects on DM in db/db mice through SIRT1/NLRP3 signalling pathway.…”

Section: Discussionmentioning

confidence: 99%

Quercetin protects against diabetic encephalopathy via SIRT1/NLRP3 pathway in db/db mice

Tian

Lü

Shi

et al. 2020

J Cellular Molecular Medi

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Epidemiological studies have found that diabetes and cognitive dysfunction are closely related. Quercetin has been certified with the effect on improving diabetes mellitus (DM) and cognitive impairment. However, the effect and related mechanism of quercetin on diabetic encephalopathy (DE) are still ambiguous. In this study, we used the db/db mice (diabetic model) to discover whether quercetin could improve DE through the Sirtuin1/NLRP3 (NOD‐, LRR‐ and pyrin domain‐containing 3) pathway. Behavioural results (Morris water maze and new object recognition tests) showed that quercetin (70 mg/kg) improved the learning and memory. Furthermore, quercetin alleviated insulin resistance and the level of fasting blood glucose. Besides, Western blot analysis also showed that quercetin increased the protein expressions of nerve‐ and synapse‐related protein, including postsynapticdensity 93 (PSD93), postsynapticdensity 95 (PSD95), brain‐derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in the brain of db/db mice. Quercetin also increased the protein expression of SIRT1 and decreased the expression of NLRP3 inflammation‐related proteins, including NLRP3, the adaptor protein ASC and cleaved Caspase‐1, the pro‐inflammatory cytokines IL‐1β and IL‐18. In conclusion, the present results indicate that the SIRT1/NLRP3 pathway may be a crucial mechanism for the neuroprotective effect of quercetin against DE.

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Section: Discussionmentioning

confidence: 99%

Quercetin protects against diabetic encephalopathy via SIRT1/NLRP3 pathway in db/db mice

Tian

Lü

Shi

et al. 2020

J Cellular Molecular Medi

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“…In endothelial cells, the NLRP3 inflammasome exhibits a significant initiating mechanism, and its activation may accelerate the development of endothelial dysfunction or atherogenic pathology by inducing plasma trimethylamine-Noxide (TMAO) [38]. The repression of the NLRP3 inflammasome is a critical factor in I/R or inflammation by correlation with SIRT1, which was proved to be involved in both preventing cells from injury induced by various stress and improving endothelial precursor cell function [39,40]. Activating the NLRP3 inflammasome signaling can promote atherosclerosis pathogenesis via the overexpression of inducible endothelial-specific GPR124 [41].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-495 Ameliorates Cardiac Microvascular Endothelial Cell Injury and Inflammatory Reaction by Suppressing the NLRP3 Inflammasome Signaling Pathway

Zhou¹,

Xiang²,

Li³

et al. 2018

Cell Physiol Biochem

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Background/Aims: In recent years, microRNA-495 (miR-495) has been reported to be a tumor-suppressor miR that is down-modulated in cancers. However, its potential mechanism remains unknown. Therefore, this study aimed to demonstrate the role of miR-495 in cardiac microvascular endothelial cell (CMEC) injury and inflammatory reaction by mediating the pyrin domain-containing 3 (NLRP3) inflammasome signaling pathway. Methods: Overall, 40 mice were assigned into myocardial ischemia/reperfusion injury (MIR) and sham groups. After model establishment, the levels of troponin T (TnT), troponin I (TnI), N-terminal pro-B-type natriuretic peptide (NT-proBNP), creatine kinase isoenzyme MB (CK-MB), myoglobin (MYO), tumor necrosis factor-alpha (TNF-α), and interleukin 1beta (IL-1β) were detected by Enzyme-Linked Immunosorbent Assay (ELISA). Apoptosis was evaluated using Terminal deoxy (d)-UTP nick end labeling (TUNEL) staining, the level of NLRP3 protein was determined by immunohistochemical assay, and miR-495 was detected by in situ hybridization (ISH). The infarct size was determined using 2, 3, 5-triphenyltetrazolium chloride (TTC) staining. The expression of miR-495 and the mRNA and protein levels of NLRP3, TNF-α, IL-1β, IL-18 and caspase-1 were evaluated by RT-qPCR and western blot analysis. After transfection, the cells were treated with a miR-495 mimic, a miR-495 inhibitor, or siNLRP3. Cell proliferation was measured by the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay and cell cycle and apoptosis by flow cytometry. Results: Mice with myocardial I/R injury had elevated levels of TnT, TnI, NT-proBNP, CK-MB, MYO, TNF-α and IL-1β; enhanced cell apoptosis; increased expression of NLRP3, TNF-α, IL-1β, IL-18 and caspase-1; and decreased miR-495 expression. MiR-495 was confirmed to target NLRP3. Moreover, miR-495 reduced the mRNA and protein levels of NLRP3, TNF-α, IL-1β, IL-18 and caspase-1, inhibited cell apoptosis and decreased cells at the G₀/G₁ phase while improving cell proliferation and increasing cells at the S phase. However, the effects of NLRP4 were proved to be reciprocal. Conclusion: In conclusion, the current study indicated that miR-495 improved CMEC injury and inflammation by suppressing the NLRP3 inflammasome signaling pathway.

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“…Salidroside also exerted its anti-inflammatory effect by inhibiting the production of pro-inflammatory cytokines (TNF-α, IL-1β and IL-6) through the blocking of the NF-κB and MAPK signaling pathways both in vitro in RAW 264.7 macrophages and in vivo in mice challenged with lipopolysaccharide [134, 135]. Further studies revealed that salidroside inhibited the activation of NLRP3 inflammasome and subsequent caspase-1 cleavage as well as IL-1β secretion both in vivo and in vitro through up-regulation of SIRT1 expression [136]. In addition, salidroside can inhibit the JAK2-STAT3 pathway by suppressing nuclear localization of STAT3 [137].…”

Section: Mechanisms Of Rhodiola Rosea L and Its Active Componentsmentioning

confidence: 99%

Rhodiola rosea L.: an Herb with Anti-Stress, Anti-Aging, and Immunostimulating Properties for Cancer Chemoprevention

Li¹,

Pham

Bui³

et al. 2017

Curr Pharmacol Rep

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Purpose of review Rhodiola rosea extracts have been used as a dietary supplement in healthy populations, including athletes, to non-specifically enhance the natural resistance of the body to both physical and behavior stresses for fighting fatigue and depression. We summarize the information with respect to the new pharmacological activities of Rhodiola rosea extracts and its underlying molecular mechanisms in this review article. Recent findings In addition to its multiplex stress-protective activity, Rhodiola rosea extracts have recently demonstrated its anti-aging, anti-inflammation, immunostimulating, DNA repair and anti-cancer effects in different model systems. Molecular mechanisms of Rhodiola rosea extracts’s action have been studied mainly along with one of its bioactive compounds, salidroside. Both Rhodiola rosea extracts and salidroside have contrast molecular mechanisms on cancer and normal physiological functions. For cancer, Rhodiola rosea extracts and salidroside inhibit the mTOR pathway and reduce angiogenesis through down-regulation of the expression of HIF-1α/HIF-2α. For normal physiological functions, Rhodiola rosea extracts and salidroside activate the mTOR pathway, stimulate paracrine function and promote neovascularization by inhibiting PHD3 and stabilizing HIF-1α proteins in skeletal muscles. In contrast to many natural compounds, salidroside is water-soluble and highly bioavailable via oral administration and concentrated in urine by kidney excretion. Summary Rhodiola rosea extracts and salidroside can impose cellular and systemic benefits similar to the effect of positive lifestyle interventions to normal physiological functions and for anti-cancer. The unique pharmacological properties of Rhodiola rosea extracts or salidroside deserve further investigation for cancer chemoprevention, in particular for human urinary bladder cancer.

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Salidroside Attenuates Ventilation Induced Lung Injury via SIRT1-Dependent Inhibition of NLRP3 Inflammasome

Cited by 44 publications

References 57 publications

Quercetin protects against diabetic encephalopathy via SIRT1/NLRP3 pathway in db/db mice

Quercetin protects against diabetic encephalopathy via SIRT1/NLRP3 pathway in db/db mice

MicroRNA-495 Ameliorates Cardiac Microvascular Endothelial Cell Injury and Inflammatory Reaction by Suppressing the NLRP3 Inflammasome Signaling Pathway

Rhodiola rosea L.: an Herb with Anti-Stress, Anti-Aging, and Immunostimulating Properties for Cancer Chemoprevention

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