The bioinformatics and metabolomics research on anti-hypoxic molecular mechanisms of Salidroside
Salidroside (SAL), a major bioactive compound of Rhodiola crenulata, has significant anti-hypoxia effect, however, its underlying molecular mechanism has not been elucidated. In order to explore the protective mechanism of SAL, the lactate dehydrogenase (LDH), reactive oxygen species (ROS), superoxi...
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Gespeichert in:
| Autor*in: |
WU, Yi [verfasserIn] MA, Yi [verfasserIn] LI, Jing [verfasserIn] ZHOU, Xue-Lin [verfasserIn] LI, Lei [verfasserIn] XU, Ping-Xiang [verfasserIn] LI, Xiao-Rong [verfasserIn] XUE, Ming [verfasserIn] |
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| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2021 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: No title available - 19, Seite 442-453 |
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volume:19 ; pages:442-453 |
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10.1016/S1875-5364(21)60043-2 |
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| 520 | |a Salidroside (SAL), a major bioactive compound of Rhodiola crenulata, has significant anti-hypoxia effect, however, its underlying molecular mechanism has not been elucidated. In order to explore the protective mechanism of SAL, the lactate dehydrogenase (LDH), reactive oxygen species (ROS), superoxide dismutase (SOD) and hypoxia-induced factor 1α (HIF-1α) were measured to establish the PC12 cell hypoxic model. Cell staining and cell viability analyses were performed to evaluate the protective effects of SAL. The metabolomics and bioinformatics methods were used to explore the protective effects of salidroside under hypoxia condition. The metabolite-protein interaction networks were further established and the protein expression level was examined by Western blotting. The results showed that 59 endogenous metabolites changed and the expression of the hub proteins of CK2, p-PTEN/PTEN, PI3K, p-Akt/Akt, NF-κB p65 and Bcl-2 were increased, suggesting that SAL could increase the expression of CK2, which induced the phosphorylation and inactivation of PTEN, reduced the inhibitory effect on PI3K signaling pathways and activated the PI3K/Akt/NF-κB survival signaling pathway. Our study provided an important insight to reveal the protective molecular mechanism of SAL as a novel drug candidate. | ||
| 650 | 4 | |a Salidroside | |
| 650 | 4 | |a Hypoxia | |
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| 650 | 4 | |a PI3K/Akt/NF- | |
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| 700 | 1 | |a ZHOU, Xue-Lin |e verfasserin |4 aut | |
| 700 | 1 | |a LI, Lei |e verfasserin |4 aut | |
| 700 | 1 | |a XU, Ping-Xiang |e verfasserin |4 aut | |
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10.1016/S1875-5364(21)60043-2 doi (DE-627)ELV006132693 (ELSEVIER)S1875-5364(21)60043-2 DE-627 ger DE-627 rda eng WU, Yi verfasserin aut The bioinformatics and metabolomics research on anti-hypoxic molecular mechanisms of Salidroside 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Salidroside (SAL), a major bioactive compound of Rhodiola crenulata, has significant anti-hypoxia effect, however, its underlying molecular mechanism has not been elucidated. In order to explore the protective mechanism of SAL, the lactate dehydrogenase (LDH), reactive oxygen species (ROS), superoxide dismutase (SOD) and hypoxia-induced factor 1α (HIF-1α) were measured to establish the PC12 cell hypoxic model. Cell staining and cell viability analyses were performed to evaluate the protective effects of SAL. The metabolomics and bioinformatics methods were used to explore the protective effects of salidroside under hypoxia condition. The metabolite-protein interaction networks were further established and the protein expression level was examined by Western blotting. The results showed that 59 endogenous metabolites changed and the expression of the hub proteins of CK2, p-PTEN/PTEN, PI3K, p-Akt/Akt, NF-κB p65 and Bcl-2 were increased, suggesting that SAL could increase the expression of CK2, which induced the phosphorylation and inactivation of PTEN, reduced the inhibitory effect on PI3K signaling pathways and activated the PI3K/Akt/NF-κB survival signaling pathway. Our study provided an important insight to reveal the protective molecular mechanism of SAL as a novel drug candidate. Salidroside Hypoxia PC12 Metabolomics PTEN PI3K/Akt/NF- MA, Yi verfasserin aut LI, Jing verfasserin aut ZHOU, Xue-Lin verfasserin aut LI, Lei verfasserin aut XU, Ping-Xiang verfasserin aut LI, Xiao-Rong verfasserin aut XUE, Ming verfasserin aut Enthalten in No title available 19, Seite 442-453 (DE-627)574362789 1875-5364 nnns volume:19 pages:442-453 GBV_USEFLAG_U SYSFLAG_U GBV_ELV GBV_ILN_2004 GBV_ILN_2015 AR 19 442-453 |
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10.1016/S1875-5364(21)60043-2 doi (DE-627)ELV006132693 (ELSEVIER)S1875-5364(21)60043-2 DE-627 ger DE-627 rda eng WU, Yi verfasserin aut The bioinformatics and metabolomics research on anti-hypoxic molecular mechanisms of Salidroside 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Salidroside (SAL), a major bioactive compound of Rhodiola crenulata, has significant anti-hypoxia effect, however, its underlying molecular mechanism has not been elucidated. In order to explore the protective mechanism of SAL, the lactate dehydrogenase (LDH), reactive oxygen species (ROS), superoxide dismutase (SOD) and hypoxia-induced factor 1α (HIF-1α) were measured to establish the PC12 cell hypoxic model. Cell staining and cell viability analyses were performed to evaluate the protective effects of SAL. The metabolomics and bioinformatics methods were used to explore the protective effects of salidroside under hypoxia condition. The metabolite-protein interaction networks were further established and the protein expression level was examined by Western blotting. The results showed that 59 endogenous metabolites changed and the expression of the hub proteins of CK2, p-PTEN/PTEN, PI3K, p-Akt/Akt, NF-κB p65 and Bcl-2 were increased, suggesting that SAL could increase the expression of CK2, which induced the phosphorylation and inactivation of PTEN, reduced the inhibitory effect on PI3K signaling pathways and activated the PI3K/Akt/NF-κB survival signaling pathway. Our study provided an important insight to reveal the protective molecular mechanism of SAL as a novel drug candidate. Salidroside Hypoxia PC12 Metabolomics PTEN PI3K/Akt/NF- MA, Yi verfasserin aut LI, Jing verfasserin aut ZHOU, Xue-Lin verfasserin aut LI, Lei verfasserin aut XU, Ping-Xiang verfasserin aut LI, Xiao-Rong verfasserin aut XUE, Ming verfasserin aut Enthalten in No title available 19, Seite 442-453 (DE-627)574362789 1875-5364 nnns volume:19 pages:442-453 GBV_USEFLAG_U SYSFLAG_U GBV_ELV GBV_ILN_2004 GBV_ILN_2015 AR 19 442-453 |
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10.1016/S1875-5364(21)60043-2 doi (DE-627)ELV006132693 (ELSEVIER)S1875-5364(21)60043-2 DE-627 ger DE-627 rda eng WU, Yi verfasserin aut The bioinformatics and metabolomics research on anti-hypoxic molecular mechanisms of Salidroside 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Salidroside (SAL), a major bioactive compound of Rhodiola crenulata, has significant anti-hypoxia effect, however, its underlying molecular mechanism has not been elucidated. In order to explore the protective mechanism of SAL, the lactate dehydrogenase (LDH), reactive oxygen species (ROS), superoxide dismutase (SOD) and hypoxia-induced factor 1α (HIF-1α) were measured to establish the PC12 cell hypoxic model. Cell staining and cell viability analyses were performed to evaluate the protective effects of SAL. The metabolomics and bioinformatics methods were used to explore the protective effects of salidroside under hypoxia condition. The metabolite-protein interaction networks were further established and the protein expression level was examined by Western blotting. The results showed that 59 endogenous metabolites changed and the expression of the hub proteins of CK2, p-PTEN/PTEN, PI3K, p-Akt/Akt, NF-κB p65 and Bcl-2 were increased, suggesting that SAL could increase the expression of CK2, which induced the phosphorylation and inactivation of PTEN, reduced the inhibitory effect on PI3K signaling pathways and activated the PI3K/Akt/NF-κB survival signaling pathway. Our study provided an important insight to reveal the protective molecular mechanism of SAL as a novel drug candidate. Salidroside Hypoxia PC12 Metabolomics PTEN PI3K/Akt/NF- MA, Yi verfasserin aut LI, Jing verfasserin aut ZHOU, Xue-Lin verfasserin aut LI, Lei verfasserin aut XU, Ping-Xiang verfasserin aut LI, Xiao-Rong verfasserin aut XUE, Ming verfasserin aut Enthalten in No title available 19, Seite 442-453 (DE-627)574362789 1875-5364 nnns volume:19 pages:442-453 GBV_USEFLAG_U SYSFLAG_U GBV_ELV GBV_ILN_2004 GBV_ILN_2015 AR 19 442-453 |
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10.1016/S1875-5364(21)60043-2 doi (DE-627)ELV006132693 (ELSEVIER)S1875-5364(21)60043-2 DE-627 ger DE-627 rda eng WU, Yi verfasserin aut The bioinformatics and metabolomics research on anti-hypoxic molecular mechanisms of Salidroside 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Salidroside (SAL), a major bioactive compound of Rhodiola crenulata, has significant anti-hypoxia effect, however, its underlying molecular mechanism has not been elucidated. In order to explore the protective mechanism of SAL, the lactate dehydrogenase (LDH), reactive oxygen species (ROS), superoxide dismutase (SOD) and hypoxia-induced factor 1α (HIF-1α) were measured to establish the PC12 cell hypoxic model. Cell staining and cell viability analyses were performed to evaluate the protective effects of SAL. The metabolomics and bioinformatics methods were used to explore the protective effects of salidroside under hypoxia condition. The metabolite-protein interaction networks were further established and the protein expression level was examined by Western blotting. The results showed that 59 endogenous metabolites changed and the expression of the hub proteins of CK2, p-PTEN/PTEN, PI3K, p-Akt/Akt, NF-κB p65 and Bcl-2 were increased, suggesting that SAL could increase the expression of CK2, which induced the phosphorylation and inactivation of PTEN, reduced the inhibitory effect on PI3K signaling pathways and activated the PI3K/Akt/NF-κB survival signaling pathway. Our study provided an important insight to reveal the protective molecular mechanism of SAL as a novel drug candidate. Salidroside Hypoxia PC12 Metabolomics PTEN PI3K/Akt/NF- MA, Yi verfasserin aut LI, Jing verfasserin aut ZHOU, Xue-Lin verfasserin aut LI, Lei verfasserin aut XU, Ping-Xiang verfasserin aut LI, Xiao-Rong verfasserin aut XUE, Ming verfasserin aut Enthalten in No title available 19, Seite 442-453 (DE-627)574362789 1875-5364 nnns volume:19 pages:442-453 GBV_USEFLAG_U SYSFLAG_U GBV_ELV GBV_ILN_2004 GBV_ILN_2015 AR 19 442-453 |
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10.1016/S1875-5364(21)60043-2 doi (DE-627)ELV006132693 (ELSEVIER)S1875-5364(21)60043-2 DE-627 ger DE-627 rda eng WU, Yi verfasserin aut The bioinformatics and metabolomics research on anti-hypoxic molecular mechanisms of Salidroside 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Salidroside (SAL), a major bioactive compound of Rhodiola crenulata, has significant anti-hypoxia effect, however, its underlying molecular mechanism has not been elucidated. In order to explore the protective mechanism of SAL, the lactate dehydrogenase (LDH), reactive oxygen species (ROS), superoxide dismutase (SOD) and hypoxia-induced factor 1α (HIF-1α) were measured to establish the PC12 cell hypoxic model. Cell staining and cell viability analyses were performed to evaluate the protective effects of SAL. The metabolomics and bioinformatics methods were used to explore the protective effects of salidroside under hypoxia condition. The metabolite-protein interaction networks were further established and the protein expression level was examined by Western blotting. The results showed that 59 endogenous metabolites changed and the expression of the hub proteins of CK2, p-PTEN/PTEN, PI3K, p-Akt/Akt, NF-κB p65 and Bcl-2 were increased, suggesting that SAL could increase the expression of CK2, which induced the phosphorylation and inactivation of PTEN, reduced the inhibitory effect on PI3K signaling pathways and activated the PI3K/Akt/NF-κB survival signaling pathway. Our study provided an important insight to reveal the protective molecular mechanism of SAL as a novel drug candidate. Salidroside Hypoxia PC12 Metabolomics PTEN PI3K/Akt/NF- MA, Yi verfasserin aut LI, Jing verfasserin aut ZHOU, Xue-Lin verfasserin aut LI, Lei verfasserin aut XU, Ping-Xiang verfasserin aut LI, Xiao-Rong verfasserin aut XUE, Ming verfasserin aut Enthalten in No title available 19, Seite 442-453 (DE-627)574362789 1875-5364 nnns volume:19 pages:442-453 GBV_USEFLAG_U SYSFLAG_U GBV_ELV GBV_ILN_2004 GBV_ILN_2015 AR 19 442-453 |
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The bioinformatics and metabolomics research on anti-hypoxic molecular mechanisms of Salidroside |
| abstract |
Salidroside (SAL), a major bioactive compound of Rhodiola crenulata, has significant anti-hypoxia effect, however, its underlying molecular mechanism has not been elucidated. In order to explore the protective mechanism of SAL, the lactate dehydrogenase (LDH), reactive oxygen species (ROS), superoxide dismutase (SOD) and hypoxia-induced factor 1α (HIF-1α) were measured to establish the PC12 cell hypoxic model. Cell staining and cell viability analyses were performed to evaluate the protective effects of SAL. The metabolomics and bioinformatics methods were used to explore the protective effects of salidroside under hypoxia condition. The metabolite-protein interaction networks were further established and the protein expression level was examined by Western blotting. The results showed that 59 endogenous metabolites changed and the expression of the hub proteins of CK2, p-PTEN/PTEN, PI3K, p-Akt/Akt, NF-κB p65 and Bcl-2 were increased, suggesting that SAL could increase the expression of CK2, which induced the phosphorylation and inactivation of PTEN, reduced the inhibitory effect on PI3K signaling pathways and activated the PI3K/Akt/NF-κB survival signaling pathway. Our study provided an important insight to reveal the protective molecular mechanism of SAL as a novel drug candidate. |
| abstractGer |
Salidroside (SAL), a major bioactive compound of Rhodiola crenulata, has significant anti-hypoxia effect, however, its underlying molecular mechanism has not been elucidated. In order to explore the protective mechanism of SAL, the lactate dehydrogenase (LDH), reactive oxygen species (ROS), superoxide dismutase (SOD) and hypoxia-induced factor 1α (HIF-1α) were measured to establish the PC12 cell hypoxic model. Cell staining and cell viability analyses were performed to evaluate the protective effects of SAL. The metabolomics and bioinformatics methods were used to explore the protective effects of salidroside under hypoxia condition. The metabolite-protein interaction networks were further established and the protein expression level was examined by Western blotting. The results showed that 59 endogenous metabolites changed and the expression of the hub proteins of CK2, p-PTEN/PTEN, PI3K, p-Akt/Akt, NF-κB p65 and Bcl-2 were increased, suggesting that SAL could increase the expression of CK2, which induced the phosphorylation and inactivation of PTEN, reduced the inhibitory effect on PI3K signaling pathways and activated the PI3K/Akt/NF-κB survival signaling pathway. Our study provided an important insight to reveal the protective molecular mechanism of SAL as a novel drug candidate. |
| abstract_unstemmed |
Salidroside (SAL), a major bioactive compound of Rhodiola crenulata, has significant anti-hypoxia effect, however, its underlying molecular mechanism has not been elucidated. In order to explore the protective mechanism of SAL, the lactate dehydrogenase (LDH), reactive oxygen species (ROS), superoxide dismutase (SOD) and hypoxia-induced factor 1α (HIF-1α) were measured to establish the PC12 cell hypoxic model. Cell staining and cell viability analyses were performed to evaluate the protective effects of SAL. The metabolomics and bioinformatics methods were used to explore the protective effects of salidroside under hypoxia condition. The metabolite-protein interaction networks were further established and the protein expression level was examined by Western blotting. The results showed that 59 endogenous metabolites changed and the expression of the hub proteins of CK2, p-PTEN/PTEN, PI3K, p-Akt/Akt, NF-κB p65 and Bcl-2 were increased, suggesting that SAL could increase the expression of CK2, which induced the phosphorylation and inactivation of PTEN, reduced the inhibitory effect on PI3K signaling pathways and activated the PI3K/Akt/NF-κB survival signaling pathway. Our study provided an important insight to reveal the protective molecular mechanism of SAL as a novel drug candidate. |
| collection_details |
GBV_USEFLAG_U SYSFLAG_U GBV_ELV GBV_ILN_2004 GBV_ILN_2015 |
| title_short |
The bioinformatics and metabolomics research on anti-hypoxic molecular mechanisms of Salidroside |
| remote_bool |
true |
| author2 |
MA, Yi LI, Jing ZHOU, Xue-Lin LI, Lei XU, Ping-Xiang LI, Xiao-Rong XUE, Ming |
| author2Str |
MA, Yi LI, Jing ZHOU, Xue-Lin LI, Lei XU, Ping-Xiang LI, Xiao-Rong XUE, Ming |
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| doi_str |
10.1016/S1875-5364(21)60043-2 |
| up_date |
2024-07-06T20:20:09.257Z |
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