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Magnetic Isolation of Microglial Cells from Neonate Mouse for Primary Cell Cultures
Published on: July 25, 2022
Remifentanil inhibits the inflammatory response of BV2 microglia and protects PC12 cells from damage caused by
Yankui Huang1, Qingxiang Cai1, Huihui Liu1
1Department of Anesthesiology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, P.R. China.
Abstract:
Microglia acts as a critical player in neuroinflammation and neuronal injury. Remifentanil (Rem) has been reported to exert anti-inflammatory activity in several types of diseases. However, the role of Rem in microglia-mediated neuroinflammation is unclear. The present study was designed to investigate the effects of Rem against lipopolysaccharide (LPS)-activated BV2 microglial and PC12 cell induced by activated BV2 microglia. Cell proliferative ability was assessed with cell counting kit-8 assay and cellular morphology was observed. ELISA assay was used to measure the expressions of PGE2 and inflammatory factors. The contents of p-NF-KB p65, p-IKKα/β, and COX2 were evaluated with the aid of western blot. The levels of NO and iNOS were assessed with Griess assay, qRT-PCR, and western blot. In addition, Tunel assay and western blot were performed to assess cell apoptosis. The data revealed that Rem alleviated BV2 microglial morphological injury induced by LPS. Furthermore, Rem suppressed inflammatory releases, iNOS, NO and PGE2 stimulated by LPS in activated BV2 cells. Moreover, Rem suppressed PC12 cell injury, the generations of inflammatory factors and cell apoptosis triggered by inflammatory mediators secreted from activated BV2 cells. These results suggest that Rem exhibited anti-neuroinflammatory activity in protecting PC12 cells against injury derived from LPS-stimulated BV2 microglia.
Insights
Remifentanil (Rem) protects against neuroinflammation by reducing microglial activation and inflammatory responses. This study shows Rem alleviates lipopolysaccharide-induced injury in microglial cells and protects neuronal cells from damage.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Microglia are key in neuroinflammation and neuronal damage.
- Remifentanil (Rem) has known anti-inflammatory effects, but its role in microglia-mediated neuroinflammation is unknown.
Purpose of the Study:
- To investigate the effects of Rem on lipopolysaccharide (LPS)-activated BV2 microglial cells.
- To assess Rem's protective effects on PC12 neuronal cells injured by activated microglia.
Main Methods:
- Cell counting kit-8 assay for proliferation and morphology.
- ELISA for inflammatory factors and PGE2.
- Western blot for p-NF-κB p65, p-IKKα/β, COX2, and iNOS.
- Griess assay, qRT-PCR, and western blot for NO and iNOS.
- Tunel assay and western blot for apoptosis.
Main Results:
- Rem alleviated LPS-induced morphological damage in BV2 microglia.
- Rem suppressed LPS-stimulated inflammatory releases, iNOS, NO, and PGE2 in BV2 cells.
- Rem reduced PC12 cell injury, inflammation, and apoptosis caused by microglia-derived mediators.
Conclusions:
- Remifentanil demonstrates anti-neuroinflammatory activity.
- Rem protects PC12 cells from injury induced by LPS-stimulated BV2 microglia.

