Dexmedetomidine regulates the anti-oxidation and autophagy of adipose-derived stromal cells under H 2 O 2 -induced oxidative stress through Nrf2/p62 pathway and improves the retention rate of autologous fat transplantati
Li Z., Wei Q., Li Y., Yang F., Ke C., Li T.
Animal Study, published in Front Pharmacol (2024) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Front Pharmacol (2024)
- Country
- Switzerland
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 39654626
- PMCID
- PMC11625574
- DOI
- 10.3389/fphar.2024.1453938
- Citations
- 1
Abstract (original English)
To investigate the protective mechanism of dexmedetomidine (DEX) on adipose-derived stromal cells (ADSCs) under oxidative stress model and its promotion effect on the retention rate of adipose granule transplantation by in vitro and in vivo experiments. The experiment was divided into control group, model group (ADSCs + H 2 O 2 +normal serum), DEX group (ADSCs + H 2 0 2 +DEX drug-containing serum), autophagy agonist group (ADSCs + H 2 O 2 +rapamycin (RAP)+normal serum), RAP + DEX group (ADSCs + H 2 O 2 +normal serum), RAP + DEX drug-containing serum), autophagy inhibitor group (ADSCs + H 2 O 2 +chloroquine (CQ)+normal serum), CQ + DEX group (ADSCs + H 2 O 2 +CQ + DEX drug-containing serum). HO-1, GSH-PX, SOD and CAT in ADSCs under oxidative stress model were measured. ROS fluorescence intensity and apoptosis ratio were detected. Expression of Nrf2, LC3-II/LC3-I and p62 were detected. In vivo , fat mixed with ADSCs or DEX -pretreated ADSCs was implanted subcutaneously in the lower back region of nude mice. Fat grafts were collected and analyzed at 2-, 4-, 6-, and 8-weeks post-transplantation. DEX pretreatment could reduce the expression of p62 to enhance the autophagy level of ADSCs under oxidative stress model. Additionally, cotransplantation of DEX-pretreated ADSCs with fat improved the long-term texture of fat grafts. DEX increased the fat graft survival and angiogenesis.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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