Danggui-Buxue decoction alleviated vascular senescence in mice exposed to chronic intermittent hypoxia through activating the Nrf2/HO-1 pathway
CONTEXT: As a major risk factor for cardiovascular diseases (CVD), Obstructive sleep apnea (OSA) is characterized by chronic intermittent hypoxia (CIH). Recent studies indicated that the increased cardiovascular risk in patients with OSA may be mediated by accelerated vascular senescence. Danggui-Buxue decoction (DBD) has been used for treating cardiovascular diseases, but its mechanism of vascular senescence regulation is still unclear.
OBJECTIVE: To investigate the effect of DBD on vascular senescence in mice exposed to CIH and to explore the role of the Nrf2/HO-1 pathway.
MATERIALS AND METHODS: C57BL/6N mice were randomly divided into Normoxia control group (CON), CIH (21%-5% O2, 20 times/h, 8 h/d) exposed group (CIH), and DBD treatment group (intragastrically treated with 2.34, 4.68, or 9.36 g/kg/day of DBD separately for 12 weeks as DBL, DBM, or DBH). Blood pressure, cardiac and vascular function, vascular senescence, inflammation response, oxidative stress, and Nrf2/HO-1 expression were determined.
RESULTS: DBD (4.68 and 9.36 g/kg) significantly decreased Tail-cuff blood pressure, increased left ventricular systolic function, and alleviated arterial stiffness and vasorelaxation dysfunction in mice exposed to CIH. DBD treatment reduced SA-β-gal activity, decreased p16 (0.68-fold, 0.62-fold), P21 (0.58-fold, 0.52-fold), and p53 expressions (0.67-fold, 0.65-fold), and increased SIRT1 expression (2.22-fold, 2.98-fold) in the aortic. DBD treatment decreased IL-6, NF-κB, and TNF-α expressions, decreased MDA but increased SOD levels, and increased Nrf2 (1.8-fold, 1.89-fold) and HO-1 (2.25-fold, 2.43-fold) expression.
DISCUSSION AND CONCLUSIONS: DBD could attenuate vascular senescence accelerated by CIH exposure through inhibiting inflammatory response and oxidative stress by activating the Nrf2/HO-1 pathway.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2023 |
|---|---|
| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:61 |
|---|---|
| Enthalten in: |
Pharmaceutical biology - 61(2023), 1 vom: 11. Dez., Seite 1041-1053 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Li, Dongli [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
Aging |
|---|
| Anmerkungen: |
Date Completed 12.07.2023 Date Revised 18.07.2023 published: Print Citation Status MEDLINE |
|---|
| doi: |
10.1080/13880209.2023.2230753 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM35932231X |
|---|
| LEADER | 01000naa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM35932231X | ||
| 003 | DE-627 | ||
| 005 | 20231226080626.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231226s2023 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1080/13880209.2023.2230753 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1197.xml |
| 035 | |a (DE-627)NLM35932231X | ||
| 035 | |a (NLM)37431236 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Li, Dongli |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Danggui-Buxue decoction alleviated vascular senescence in mice exposed to chronic intermittent hypoxia through activating the Nrf2/HO-1 pathway |
| 264 | 1 | |c 2023 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 12.07.2023 | ||
| 500 | |a Date Revised 18.07.2023 | ||
| 500 | |a published: Print | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a CONTEXT: As a major risk factor for cardiovascular diseases (CVD), Obstructive sleep apnea (OSA) is characterized by chronic intermittent hypoxia (CIH). Recent studies indicated that the increased cardiovascular risk in patients with OSA may be mediated by accelerated vascular senescence. Danggui-Buxue decoction (DBD) has been used for treating cardiovascular diseases, but its mechanism of vascular senescence regulation is still unclear | ||
| 520 | |a OBJECTIVE: To investigate the effect of DBD on vascular senescence in mice exposed to CIH and to explore the role of the Nrf2/HO-1 pathway | ||
| 520 | |a MATERIALS AND METHODS: C57BL/6N mice were randomly divided into Normoxia control group (CON), CIH (21%-5% O2, 20 times/h, 8 h/d) exposed group (CIH), and DBD treatment group (intragastrically treated with 2.34, 4.68, or 9.36 g/kg/day of DBD separately for 12 weeks as DBL, DBM, or DBH). Blood pressure, cardiac and vascular function, vascular senescence, inflammation response, oxidative stress, and Nrf2/HO-1 expression were determined | ||
| 520 | |a RESULTS: DBD (4.68 and 9.36 g/kg) significantly decreased Tail-cuff blood pressure, increased left ventricular systolic function, and alleviated arterial stiffness and vasorelaxation dysfunction in mice exposed to CIH. DBD treatment reduced SA-β-gal activity, decreased p16 (0.68-fold, 0.62-fold), P21 (0.58-fold, 0.52-fold), and p53 expressions (0.67-fold, 0.65-fold), and increased SIRT1 expression (2.22-fold, 2.98-fold) in the aortic. DBD treatment decreased IL-6, NF-κB, and TNF-α expressions, decreased MDA but increased SOD levels, and increased Nrf2 (1.8-fold, 1.89-fold) and HO-1 (2.25-fold, 2.43-fold) expression | ||
| 520 | |a DISCUSSION AND CONCLUSIONS: DBD could attenuate vascular senescence accelerated by CIH exposure through inhibiting inflammatory response and oxidative stress by activating the Nrf2/HO-1 pathway | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Obstructive sleep apnea | |
| 650 | 4 | |a aging | |
| 650 | 4 | |a inflammation | |
| 650 | 4 | |a oxidative stress | |
| 650 | 7 | |a NF-E2-Related Factor 2 |2 NLM | |
| 700 | 1 | |a Si, Jianchao |e verfasserin |4 aut | |
| 700 | 1 | |a Guo, Yajing |e verfasserin |4 aut | |
| 700 | 1 | |a Liu, Bingbing |e verfasserin |4 aut | |
| 700 | 1 | |a Chen, Xue |e verfasserin |4 aut | |
| 700 | 1 | |a Qi, Kerong |e verfasserin |4 aut | |
| 700 | 1 | |a Yang, Shengchang |e verfasserin |4 aut | |
| 700 | 1 | |a Ji, Ensheng |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Pharmaceutical biology |d 1997 |g 61(2023), 1 vom: 11. Dez., Seite 1041-1053 |w (DE-627)NLM097504416 |x 1744-5116 |7 nnns |
| 773 | 1 | 8 | |g volume:61 |g year:2023 |g number:1 |g day:11 |g month:12 |g pages:1041-1053 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1080/13880209.2023.2230753 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 61 |j 2023 |e 1 |b 11 |c 12 |h 1041-1053 | ||