Salidroside inhibits MAPK, NF-κB, and STAT3 pathways in psoriasis-associated oxidative stress via SIRT1 activation

Xu, Fengli; Xu, Jixiang; Xiong, Xia; Deng, Yongqiong

doi:10.1080/13510002.2019.1658377

Cited by 161 publications

(111 citation statements)

References 72 publications

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“…40 Meanwhile, ROS can regulate the MAPK, STAT3, NF-κB, and AKT signaling pathways, which are involved in apoptosis, proliferation, and other life processes. 41,42 In this study, kaempferide increased ROS levels, which led to the regulation of downstream signaling pathways and promoted cell apoptosis. However, when the cells were treated with NAC and kaempferide, NAC had no effect on the control group, but had a strong inhibitory effect on the kaempferide group.…”

Section: Discussionmentioning

confidence: 58%

Kaempferide Induces G0/G1 Phase Arrest and Apoptosis via ROS-Mediated Signaling Pathways in A549 Human Lung Cancer Cells

Luo

et al. 2020

Natural Product Communications

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Kaempferide is an O-methylated flavonol that has received much attention due to its various biological activities. In this study, we explored the underlying mechanisms of kaempferide in human lung cancer A549 cells. The Cell Counting Kit-8 (CCK-8) assay, Hoechst 33342/propidium iodide double staining, flow cytometry, scratch wound healing assay, and Western blot analysis were used to measure cell apoptosis, the cell cycle, reactive oxygen species (ROS) levels, and cell migration of human lung cancer cells. Kaempferide significantly inhibited human lung cancer cell proliferation, and its toxic effects on normal cells were significantly lower than those of 5-fluorouracil. Kaempferide induced A549 cell apoptosis by decreasing the mitochondrial membrane potential and the expression level of B-cell lymphoma 2, and by increasing the expression levels of Bcl-2-associated X protein and caspase-3. It also regulated mitogen-activated protein kinase (MAPK), signal transducer and activator of transcription 3 (STAT3), and nuclear factor kappa B (NF-κB) signaling pathways by increasing the expression levels of phosphorylated c-Jun N-terminal kinase, p-p38, I kappa B, and by decreasing the expression levels of phosphorylated extracellular signal-regulated kinase, p-STAT3, and NF-κB. Kaempferide induced cell cycle arrest in the G0/G1 phase in A549 cells by downregulating the expression levels of p-AKT, cyclin D1, and cyclin-dependent kinase 2. Furthermore, kaempferide blocked A549 cell migration by downregulating the expression levels of transforming growth factor beta 1 (TGF-β1), p-β-catenin, p-glycogen synthase kinase 3 beta, N-cadherin, and vimentin, and by upregulating the expression level of E-cadherin. Kaempferide enhanced the accumulation of ROS, and N-acetyl-l-cysteine (a ROS inhibitor) decreased the regulation of MAPK, NF-κB, AKT, and TGF-β signaling pathways by kaempferide, inhibited cell apoptosis, and reversed cell cycle arrest. Our results showed that kaempferide induced apoptosis via ROS-mediated MAPK, NF-κB, AKT, and TGF-β signaling pathways in A549 cells. Thus, kaempferide may be a novel drug candidate for lung cancer.

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Section: Discussionmentioning

confidence: 58%

Kaempferide Induces G0/G1 Phase Arrest and Apoptosis via ROS-Mediated Signaling Pathways in A549 Human Lung Cancer Cells

Luo

et al. 2020

Natural Product Communications

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“…MAPK signaling pathway, including P38 and JNK, mediates cell apoptosis through combining a complex with a proapoptotic factor of p53 [31]. In addition, it can motivate the expression of in ammatory factors mediated through NF-κB signaling pathways and accelerate the kidney pathological changes [32]. HIF-1 was increased in DN mice, which mediates DN-induced kidney brotic disease [33].…”

Section: Discussionmentioning

confidence: 99%

Network Pharmacology Study Reveals the Mechanism of Astragali Radix in Treatment of Diabetic Nephropathy

Tian¹,

Chen²,

Chen³

et al. 2020

Preprint

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Background Diabetic nephropathy (DN), a unique complication of diabetes, could contribute to an increase in mortality. In this study, we predicted and proved the molecular pharmacological mechanism concerning the protective effects of Astragali Radix on DN. Methods The same potential target genes from Astragali Radix and DN were analyzed and constructed the protein interaction network. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment-related major targets and signal pathways were performed. The drug-ingredients-target-disease network was visually built using Cytoscape 3.6.1. The beneficial pharmacological activities of quercetin from Astragali Radix were confirmed by CCK-8 assay, determination of antioxidant parameters and Western blotting analysis. Results There are 12 bioactive components from Astragali Radix and 56 same targets between Astragali Radix and DN. The GO analysis results showed that the biological processes mainly included protein homodimerization activity. KEGG analysis indicate that the screened targets were most closely linked to the mitogen-activated protein kinase (MAPK) signaling pathway. The drug-ingredients-target-disease network results revealed that the therapeutic effects of Astragali Radix mainly included oxidative stress, inflammatory reaction and apoptosis. During the verification process, quercetin from Astragali Radix could attenuate cytotoxicity, enhance catalase (CAT) and superoxide dismutase (SOD) activities and suppress MAPK signaling pathway. Conclusions In the current study, network pharmacology with experimental analysis predicted and proved the therapeutic function of Astragali Radix by improving antioxidant capacity and suppressing MAPK signaling pathway, these investigations could provide a new perspective for further exploration of Astragali Radix on DN treatment.

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“…Sirtuin 1 (SIRT1) belongs to a family of proteins that perform important functions in the process of metabolism or the cell cycle. Important from the point of view of Ps are their functions associated with inflammation, proliferation, or apoptosis [ 90 ]. SIRT1, as an NAD-dependent deacetylase, inhibits inflammation, excessive keratinocyte proliferation, and angiogenesis.…”

Section: Perspective Markers Of Oxidative Stress In Psmentioning

confidence: 99%

“…SIRT1, as an NAD-dependent deacetylase, inhibits inflammation, excessive keratinocyte proliferation, and angiogenesis. In addition, its activation supports the inhibition of MAP or NF-kB kinase pathways, whose importance is in the process of oxidative stress and pathogenesis of Ps [ 90 ]. The literature indicates the significance of SIRT1 in the differentiation of keratinocytes, while inhibiting their hyperproliferation, as is the case with Ps.…”

Section: Perspective Markers Of Oxidative Stress In Psmentioning

confidence: 99%

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Oxidative Stress as an Important Contributor to the Pathogenesis of Psoriasis

Pleńkowska

Gabig-Cimińska

Mozolewski

2020

IJMS

121

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This review discusses how oxidative stress (OS), an imbalance between oxidants and antioxidants in favor of the oxidants, increased production of reactive oxygen species (ROS)/reactive nitrogen species (RNS), and decreased concentration/activity of antioxidants affect the pathogenesis or cause the enhancement of psoriasis (Ps). Here, we also consider how ROS/RNS-induced stress modulates the activity of transcriptional factors and regulates numerous protein kinase cascades that participate in the regulation of crosstalk between autophagy, apoptosis, and regeneration. Answers to these questions will likely uncover novel strategies for the treatment of Ps. Action in the field will avoid destructive effects of ROS/RNS-mediated OS resulting in cellular dysfunction and cell death. The combination of the fragmentary information on the role of OS can provide evidence to extend the full picture of Ps.

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Salidroside inhibits MAPK, NF-κB, and STAT3 pathways in psoriasis-associated oxidative stress via SIRT1 activation

Cited by 161 publications

References 72 publications

Kaempferide Induces G0/G1 Phase Arrest and Apoptosis via ROS-Mediated Signaling Pathways in A549 Human Lung Cancer Cells

Kaempferide Induces G0/G1 Phase Arrest and Apoptosis via ROS-Mediated Signaling Pathways in A549 Human Lung Cancer Cells

Network Pharmacology Study Reveals the Mechanism of Astragali Radix in Treatment of Diabetic Nephropathy

Oxidative Stress as an Important Contributor to the Pathogenesis of Psoriasis

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