# Curcumin ameliorates ischemic stroke injury by downregulating GMFB expression: An in vitro study

**Authors:** Xiumei Bai, Yabin Song, Xiangyan Zhang, Liqiong Liu, Haixia Wu, Jiaqing Feng, Lihong Wu, Huizhen Liu, Diangui Zhou

PMC · DOI: 10.17305/bb.2024.10957 · Biomolecules and Biomedicine · 2024-09-26

## TL;DR

This study shows that curcumin reduces brain cell damage from stroke by lowering GMFB levels in a lab model.

## Contribution

The novel finding is that curcumin ameliorates ischemic stroke injury by downregulating GMFB expression in vitro.

## Key findings

- Curcumin reduces OGD/R-induced cell damage by downregulating GMFB expression.
- GMFB overexpression worsens cell viability, increases ROS and apoptosis in OGD/R models.
- Silencing GMFB ameliorates OGD/R-induced cell damage.

## Abstract

Ischemic stroke (IS) is a cerebrovascular sickness, and cerebral ischemia–reperfusion (I/R) damage often occurs, but there is still a lack of drugs that can significantly alleviate it. Curcumin (Cur) exerts pharmacological effects, such as antioxidative stress, anti-inflammation, and the promotion of apoptosis through regulating various pathways, but its efficacy and specific mechanism of action in IS have not been fully clarified. The purpose of this paper is to study the influence of Cur on IS. Brain microvascular endothelial cells (BMECs) were used to create an oxygen–glucose deprivation/reoxygenation (OGD/R) model to simulate I/R damage. The cell viability was assessed using an MTT assay. The LDH level and ROS positive rate were measured using commercial kits. The cell invasion was examined using a transwell assay. The apoptosis was assessed by flow cytometry. The contents of glia maturation factor beta (GMFB), Bax, and Bcl2 were measured using western blot. We confirmed that in the OGD/R-induced IS cell model, the abundance of GMFB was enhanced in the OGD/R group vs the control group. GMFB overexpression promoted OGD/R-induced cell viability diminution, increased LDH and ROS levels, lessened cell invasion ability, enhanced cell apoptosis, enhanced Bax levels, and decreased Bcl2 levels. Silencing GMFB ameliorated OGD/R-induced cell damage. Cur ameliorated OGD/R-induced cell damage. Cur curbed OGD/R-induced cell damage by downregulating GMFB expression. In conclusion, Cur cured IS-induced cell damage by downregulating GMFB expression.

## Linked entities

- **Genes:** GMFB (glia maturation factor beta) [NCBI Gene 2764], BAX (BCL2 associated X, apoptosis regulator) [NCBI Gene 581], BCL2 (BCL2 apoptosis regulator) [NCBI Gene 596]
- **Chemicals:** curcumin (PubChem CID 969516)
- **Diseases:** ischemic stroke (MONDO:1060198)

## Full-text entities

- **Genes:** GMFB (glia maturation factor beta) [NCBI Gene 2764] {aka GMF}, BAX (BCL2 associated X, apoptosis regulator) [NCBI Gene 581] {aka BCL2L4}, BCL2 (BCL2 apoptosis regulator) [NCBI Gene 596] {aka Bcl-2, PPP1R50}
- **Diseases:** cerebral ischemia-reperfusion (I/R) damage (MESH:D015427), R (MESH:C580424), inflammation (MESH:D007249), IS (MESH:D002544), cerebrovascular sickness (MESH:D002561), OGD (MESH:C536050)

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12010991/full.md

## References

20 references — full list in the complete paper: https://tomesphere.com/paper/PMC12010991/full.md

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Source: https://tomesphere.com/paper/PMC12010991