Related Experiment Video
Updated: Feb 6, 2026
Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
Published on: August 23, 2024
Propofol attenuates mast cell degranulation via inhibiting the miR-221/PI3K/Akt/Ca2+ pathway
Zhiyong Yi1, Zhipan Yi2, Kai Huang1
1Department of Human Anatomy and Histology-Embryology, Medical School, Shaoyang University, Shaoyang, Hunan 422000, P.R. China.
Abstract:
The aim of the present study was to investigate the effect of propofol on immunoglobulin (Ig)E-activated mast cell degranulation and explore the underlying mechanisms responsible. RBL-2H3 cells were treated with propofol for at a variety of concentrations and different amounts of time. Cell viability was assessed using an MTT assay and microRNA (miR)-221 expression was quantified using reverse transcription-quantitative polymerase chain reaction. RBL-2H3 cells were transfected with miR-221 mimic or a negative control and degranulation, including the release of β-hexosaminidase and histamine, was evaluated using an ELISA kit. The effect of miR-221 overexpression on the phosphorylation of protein kinase B (Akt) was detected using western blotting and extracellular Ca2+ influx was measured via afura-2 assay. The phosphoinositide 3-kinase(PI3K) inhibitor LY294002 was used to investigate the association between PI3K/Akt signaling and Ca2+ influx in the presence of propofol. The results demonstrated that propofol treatment suppressed RBL-2H3 cell proliferation in a dose- and time-dependent manner. Propofol inhibited miR-221 expression in a dose-dependent manner compared with the control group; however, the inhibitive effect was significantly abrogated following transfection with miR-221 mimics. Furthermore, β-hexosaminidase and histamine release, PI3K/Akt signaling and Ca2+ influx were decreased following propofol application. miR-221 overexpression markedly ameliorated the suppressive effect of propofol. Treatment with LY294002 reversed the propofol-induced decrement of Ca2+ influx on IgE-mediated RBL-2H3 cells, suggesting an association between PI3K/Akt signaling and Ca2+ influx. In conclusion, the results of the present study suggest that propofol treatment attenuates mast cell degranulation via inhibiting the miR-221/PI3K/Akt/Ca2+ pathway. These results indicate that propofol may have a potential therapeutic effect as a treatment for allergic diseases.
Insights
Propofol inhibits mast cell degranulation by suppressing microRNA-221 (miR-221) and the PI3K/Akt/Ca2+ pathway. This suggests propofol may be a potential treatment for allergic diseases.
Area of Science:
- Immunology
- Pharmacology
- Molecular Biology
Background:
- Mast cells play a crucial role in allergic responses through degranulation.
- Immunoglobulin E (IgE)-mediated activation triggers mast cell degranulation, releasing inflammatory mediators.
- Understanding the molecular mechanisms regulating mast cell degranulation is vital for developing anti-allergic therapies.
Purpose of the Study:
- To investigate the effect of propofol on IgE-activated mast cell degranulation.
- To elucidate the underlying molecular mechanisms, focusing on microRNA-221 (miR-221) and the PI3K/Akt/Ca2+ signaling pathway.
Main Methods:
- RBL-2H3 cells were treated with propofol, and cell viability was assessed via MTT assay.
- microRNA-221 (miR-221) expression was quantified using RT-qPCR.
- Mast cell degranulation (β-hexosaminidase, histamine release), PI3K/Akt signaling, and Ca2+ influx were measured.
- Inhibitor studies (LY294002) and miR-221 mimics were used to explore pathway involvement.
Main Results:
- Propofol suppressed RBL-2H3 cell proliferation and inhibited miR-221 expression in a dose-dependent manner.
- Overexpression of miR-221 abrogated propofol's inhibitory effects on degranulation.
- Propofol decreased β-hexosaminidase and histamine release, PI3K/Akt signaling, and Ca2+ influx.
- miR-221 overexpression ameliorated propofol's suppressive effects, and PI3K inhibition affected Ca2+ influx.
Conclusions:
- Propofol attenuates mast cell degranulation by inhibiting the miR-221/PI3K/Akt/Ca2+ pathway.
- These findings suggest propofol has potential therapeutic applications for allergic diseases.
- The study highlights the role of miR-221 in regulating propofol's effects on mast cells.
More Related Videos
11:31Isolation of Peritoneum-derived Mast Cells and Their Functional Characterization with Ca2+-imaging and Degranulation Assays
Published on: July 4, 2018
17:35A Microplate Assay to Assess Chemical Effects on RBL-2H3 Mast Cell Degranulation: Effects of Triclosan without Use of an Organic Solvent
Published on: November 1, 2013
Related Concept Videos
01:22PI3K/mTOR/AKT Signaling Pathway
00:46Feedback Inhibition
02:42Transcription Attenuation in Prokaryotes
There are several different mechanisms used to attenuate transcription. In ribosome mediated...
01:27C4 Pathway and CAM
C4 Pathway
The C4 pathway is used by plants such as...
01:25Antiasthma Drugs: Mast Cell Stabilizers and Anti-IgE Drugs
Mast cell stabilizers, such as cromolyn (also known as sodium cromoglycate) and nedocromil (Tilade), are effective drugs in asthma management. These stabilizers hinder histamine release by skillfully obstructing the activation of mast cells and other cellular entities. Notably, they navigate this task without...
01:30Enzyme Inhibition