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Propofol relieves inflammation in MIRI rats by inhibiting Rho/Rock signaling pathway
1Department of Anesthesiology, Affiliated Hospital of Chengde Medical College, Chengde, China. liyan0567@126.com.
Objective:
The aim of this study was to investigate the effects of propofol on myocardial ischemia-reperfusion injury (MIRI) and its mechanism by establishing in vivo rat models.
Materials And Methods:
Sprague-Dawley rats were selected for the construction of MIRI models in vivo. All rats were divided into three groups, including sham operation group (Sham operation), MIRI group and MIRI + propofol group. At 2 h after reperfusion, myocardial tissues and blood samples were collected from rats. The expression levels of serum lactic dehydrogenase (LDH) and creatine kinase-MB (CK-MB), as well as serum interleukin-6 (IL-6), IL-10 and tumor necrosis factor-α (TNF-α), were measured in each group of rats, respectively. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) assay was employed to detect the apoptosis of myocardial cells. Additionally, the messenger ribonucleic acid (mRNA) and protein expressions of Ras homolog gene family, member A (RhoA) and Rho-associated coiled-coil-containing protein kinase 2 (Rock2) were determined via quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting, respectively.
Results:
(1) The expression levels of serum LDH and CK-MB were significantly lower in MIRI + propofol group than those in MIRI group (p<0.05). (2) In comparison with MIRI group, MIRI + propofol group exhibited significantly reduced serum IL-6 and TNF-α levels (p<0.01) and elevated serum IL-10 level (p<0.01). (3) Compared with MIRI group, the apoptosis of myocardial cells was remarkably reduced in MIRI + propofol group after IRI (p<0.05). (4) The mRNA and protein expressions of RhoA and Rock2 were significantly lower in MIRI + propofol group than those in MIRI group (p<0.05).
Conclusions:
Propofol relieves MIRI and inflammation, reduces the level of oxidative stress and represses I/R-induced myocardial cell apoptosis in MIRI rats by inhibiting the activity of the Rho/Rock signaling pathway.
Insights
Propofol effectively mitigates myocardial ischemia-reperfusion injury (MIRI) in rats by reducing inflammation and cell apoptosis. This protective effect is achieved by inhibiting the Rho/Rock signaling pathway, offering a potential therapeutic strategy.
Area of Science:
- Cardiology
- Pharmacology
- Molecular Biology
Background:
- Myocardial ischemia-reperfusion injury (MIRI) is a significant clinical challenge.
- Understanding the molecular mechanisms underlying MIRI is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the protective effects of propofol against MIRI in a rat model.
- To elucidate the underlying mechanism involving the Rho/Rock signaling pathway.
Main Methods:
- Established MIRI models in Sprague-Dawley rats.
- Administered propofol to a treatment group.
- Measured serum biomarkers (LDH, CK-MB, IL-6, IL-10, TNF-α).
- Assessed myocardial cell apoptosis using TUNEL assay.
- Quantified RhoA and Rock2 expression via qRT-PCR and Western blotting.
Main Results:
- Propofol significantly reduced serum LDH and CK-MB levels.
- Propofol decreased pro-inflammatory cytokines (IL-6, TNF-α) and increased anti-inflammatory cytokine (IL-10).
- Propofol markedly reduced myocardial cell apoptosis.
- Propofol downregulated the expression of RhoA and Rock2.
Conclusions:
- Propofol demonstrates significant cardioprotective effects against MIRI.
- Propofol alleviates inflammation and oxidative stress.
- The protective mechanism involves the inhibition of the Rho/Rock signaling pathway, reducing myocardial cell apoptosis.
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