# Dynamic changes in and time sequence of ultraviolet B-induced apoptosis in rat corneal epithelial cells

**Authors:** Shaobo Du, Jiande Li, Linchi Chen, Zhanyu Niu, Lan Gao

PMC · DOI: 10.5935/0004-2749.20220042 · Arquivos Brasileiros de Oftalmologia · 2025-08-21

## TL;DR

This study examines how rat corneal epithelial cells undergo apoptosis after UVB exposure, showing rapid cell death linked to both extrinsic and intrinsic pathways.

## Contribution

The study provides a detailed time sequence of UVB-induced apoptosis in rat corneal epithelial cells, highlighting the involvement of both extrinsic and intrinsic pathways.

## Key findings

- UVB irradiation rapidly triggers apoptosis in rat corneal epithelial cells.
- Apoptosis involves both extrinsic (caspase-8, Bax) and intrinsic (mitochondrial membrane potential) pathways.
- Apoptotic rate peaks at 6 hours post-irradiation and declines afterward.

## Abstract

To systematically examine the dynamic changes and time sequence in corneal
epithelial cell apoptosis after excessive ultraviolet B irradiation.

Ultraviolet B (144 mJ/cm2) was used to irradiate rat corneal
epithelial cells for 2 h. Cell morphology was observed on differential
interference contrast microscopy, and the numbers of the different kinds of
apoptotic cells were counted using the ImageJ software. Cell viability was
measured with the 3-(4,5-dimethyl-2-thiazolyl)-2,5- diphenyl-2-H-tetrazolium
bromide method. Cell apoptotic rate and loss of mitochondrial membrane
potential were detected using flow cytometric analyses. The expression
levels of 3 apoptotic genes were measured with real-time quantitative
polymerase chain reaction at different time points within 0-24 h after
irradiation.

After 144-mJ/cm2 ultraviolet B irradiation for 2 h, the expression
levels of caspase-8 and Bax were highest at 0 h;
furthermore, the mitochondrial membrane potential decreased at 0 h and
remained constant for 6 h in a subsequent culture. At 6 h, caspase-3 was
activated. The decrease in cell viability and increase in apoptotic rate
peaked at 6 h. The caspase-3 expression level decreased within 12-24 h,
which led to a decline in apoptotic rate and change in apoptotic stage.

The corneal epithelial cells exhibited rapid apoptosis after ultraviolet B
irradiation, which was associated with both extrinsic and intrinsic
pathways.

## Linked entities

- **Genes:** casp8 (caspase 8, apoptosis-related cysteine peptidase) [NCBI Gene 58022], BAX (BCL2 associated X, apoptosis regulator) [NCBI Gene 581], Casp3 (caspase 3) [NCBI Gene 12367]
- **Species:** Rattus norvegicus (taxon 10116)

## Full-text entities

- **Genes:** Casp3 (caspase 3) [NCBI Gene 25402] {aka CPP32-beta, Lice, Yama}, Bax (BCL2 associated X, apoptosis regulator) [NCBI Gene 24887], Casp8 (caspase 8) [NCBI Gene 64044] {aka CASP-8}, CASP3 (caspase 3) [NCBI Gene 836] {aka CPP32, CPP32B, SCA-1}
- **Chemicals:** Ultraviolet B (-), 3-(4,5-dimethyl-2-thiazolyl)-2,5- diphenyl-2-H-tetrazolium bromide (MESH:C000598529)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116], Dipturus trachyderma (ray, species) [taxon 255564]

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11878396/full.md

## References

30 references — full list in the complete paper: https://tomesphere.com/paper/PMC11878396/full.md

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Source: https://tomesphere.com/paper/PMC11878396