Emodin induces apoptosis and autophagy of fibroblasts obtained from patient with ankylosing spondylitis
BACKGROUND: Ankylosing spondylitis (AS) is a type of rheumatoid disease, which has been reported to be associated with the excessive proliferation of fibroblasts recently. Emodin, a single component from a traditional Chinese medicine Rheum palmatum, exerts anti-inflammation and antirheumatic arthritis activities. However, could emodin be used to treat AS remains unclear? Thus, this study aimed to investigate the effect of emodin on AS.
METHODS: Fibroblasts obtained from patients with AS were used in the current study. In addition, multiple cellular and molecular biology techniques such as Cell Counting Kit-8, Western blotting, flow cytometry, monodansylcadaverine staining, and immunofluorescence assay were applied as well.
RESULTS: Emodin-induced apoptosis of fibroblasts obtained from patient with AS via increasing active caspase-9, active caspase-3, and Bax levels and downregulating Bcl-2. Meanwhile, emodin enhanced autophagy in fibroblasts via upregulation of the expression of Atg12, Atg5, and Beclin 1, which was further confirmed by monodansylcadaverine staining. As expected, autophagy inhibitor 3-methyladenine (3MA) completely reversed emodin-induced autophagy in fibroblasts. Moreover, 3MA significantly increased emodin-induced apoptosis of fibroblasts obtained from patient with AS by increasing the levels of γH2AX, active caspase-9, active caspase-3, and cleaved poly ADP-ribose polymerase.
CONCLUSION: Our results indicated that emodin effectively induced apoptosis and autophagy of fibroblasts obtained from patient with AS. In addition, suppression of autophagy enhanced emodin-induced apoptosis in fibroblasts. Therefore, we proposed that combination of emodin with autophagy inhibitor might be a potent strategy for improving the symptoms of AS in the future.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2019 |
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| Erschienen: |
2019 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:13 |
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| Enthalten in: |
Drug design, development and therapy - 13(2019) vom: 21., Seite 601-609 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Ma, Cong [VerfasserIn] |
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| Links: |
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| Themen: |
3MA |
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| Anmerkungen: |
Date Completed 31.07.2019 Date Revised 08.04.2022 published: Electronic-eCollection Citation Status MEDLINE |
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| doi: |
10.2147/DDDT.S182087 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM294337709 |
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| 245 | 1 | 0 | |a Emodin induces apoptosis and autophagy of fibroblasts obtained from patient with ankylosing spondylitis |
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| 500 | |a Date Revised 08.04.2022 | ||
| 500 | |a published: Electronic-eCollection | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a BACKGROUND: Ankylosing spondylitis (AS) is a type of rheumatoid disease, which has been reported to be associated with the excessive proliferation of fibroblasts recently. Emodin, a single component from a traditional Chinese medicine Rheum palmatum, exerts anti-inflammation and antirheumatic arthritis activities. However, could emodin be used to treat AS remains unclear? Thus, this study aimed to investigate the effect of emodin on AS | ||
| 520 | |a METHODS: Fibroblasts obtained from patients with AS were used in the current study. In addition, multiple cellular and molecular biology techniques such as Cell Counting Kit-8, Western blotting, flow cytometry, monodansylcadaverine staining, and immunofluorescence assay were applied as well | ||
| 520 | |a RESULTS: Emodin-induced apoptosis of fibroblasts obtained from patient with AS via increasing active caspase-9, active caspase-3, and Bax levels and downregulating Bcl-2. Meanwhile, emodin enhanced autophagy in fibroblasts via upregulation of the expression of Atg12, Atg5, and Beclin 1, which was further confirmed by monodansylcadaverine staining. As expected, autophagy inhibitor 3-methyladenine (3MA) completely reversed emodin-induced autophagy in fibroblasts. Moreover, 3MA significantly increased emodin-induced apoptosis of fibroblasts obtained from patient with AS by increasing the levels of γH2AX, active caspase-9, active caspase-3, and cleaved poly ADP-ribose polymerase | ||
| 520 | |a CONCLUSION: Our results indicated that emodin effectively induced apoptosis and autophagy of fibroblasts obtained from patient with AS. In addition, suppression of autophagy enhanced emodin-induced apoptosis in fibroblasts. Therefore, we proposed that combination of emodin with autophagy inhibitor might be a potent strategy for improving the symptoms of AS in the future | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a 3MA | |
| 650 | 4 | |a ankylosing spondylitis | |
| 650 | 4 | |a apoptosis | |
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| 650 | 4 | |a emodin | |
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| 700 | 1 | |a Shao, Pei-Pei |e verfasserin |4 aut | |
| 700 | 1 | |a Gu, Wen |e verfasserin |4 aut | |
| 700 | 1 | |a Qu, Kun |e verfasserin |4 aut | |
| 700 | 1 | |a Shi, Yang |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Bei |e verfasserin |4 aut | |
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