Ginsenoside regulates Treg/Th17 cell ratio and inhibits inflammation to treat COPD
Objective: Several studies have suggested an involvement of the immune system in the occurrence and development of chronic obstructive pulmonary disease (COPD), but the mechanism is still unclear. The aim of this study was to explore the mechanism of ginsenoside in inhibiting inflammation by regulating FOXP3 in COPD. Methods: Eighty COPD patients were selected and 35 healthy people were enrolled in the study to determine clinical efficacy, observation index, and SGRQ scores. Percentage of Treg and Th17 cells were detected by flow cytometry; HE staining was used to detect the effect of ginsenoside therapy on pathological changes of COPD in mice. Additionally, we transfected FOXP3 inhibitor; RT-PCR and western blot were used to detect the inflammation related genes and proteins. Results: The basic information of the patients were comparable. The clinical outcome in the treatment group was better than that in the control group, which indicated that ginsenoside has a certain therapeutic effect on COPD patients. The lung function and 6MWT distance results indicated that ginsenoside could stabilize the clinical symptoms of COPD patients and improve their quality of life. Flow cytometry results showed that ginsenoside can increase Treg expression while reducing Th17 cell expression. RT-PCR and western blot results showed that the expression of TNF-α and IL-17 in the model group was significantly increased after treatment, obviously caused by an increased expression of FOXP3. Conclusion: Ginsenoside can inhibit inflammation in COPD by up-regulating FOXP3.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2020 |
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| Erschienen: |
2020 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:75 |
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| Enthalten in: |
Die Pharmazie - 75(2020), 11 vom: 01. Nov., Seite 590-594 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Xu, Yan-Qiu [VerfasserIn] |
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| Links: |
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| Themen: |
Anti-Inflammatory Agents |
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| Anmerkungen: |
Date Completed 13.08.2021 Date Revised 13.08.2021 published: Print Citation Status MEDLINE |
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| doi: |
10.1691/ph.2020.0696 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM318057557 |
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| 245 | 1 | 0 | |a Ginsenoside regulates Treg/Th17 cell ratio and inhibits inflammation to treat COPD |
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| 500 | |a published: Print | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Objective: Several studies have suggested an involvement of the immune system in the occurrence and development of chronic obstructive pulmonary disease (COPD), but the mechanism is still unclear. The aim of this study was to explore the mechanism of ginsenoside in inhibiting inflammation by regulating FOXP3 in COPD. Methods: Eighty COPD patients were selected and 35 healthy people were enrolled in the study to determine clinical efficacy, observation index, and SGRQ scores. Percentage of Treg and Th17 cells were detected by flow cytometry; HE staining was used to detect the effect of ginsenoside therapy on pathological changes of COPD in mice. Additionally, we transfected FOXP3 inhibitor; RT-PCR and western blot were used to detect the inflammation related genes and proteins. Results: The basic information of the patients were comparable. The clinical outcome in the treatment group was better than that in the control group, which indicated that ginsenoside has a certain therapeutic effect on COPD patients. The lung function and 6MWT distance results indicated that ginsenoside could stabilize the clinical symptoms of COPD patients and improve their quality of life. Flow cytometry results showed that ginsenoside can increase Treg expression while reducing Th17 cell expression. RT-PCR and western blot results showed that the expression of TNF-α and IL-17 in the model group was significantly increased after treatment, obviously caused by an increased expression of FOXP3. Conclusion: Ginsenoside can inhibit inflammation in COPD by up-regulating FOXP3 | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Randomized Controlled Trial | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
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| 650 | 7 | |a FOXP3 protein, human |2 NLM | |
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| 700 | 1 | |a Shi, Suo -Fang |e verfasserin |4 aut | |
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