Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Catalpol represses the migration, proliferation and epithelial-mesenchymal transition of TGF-β2-stimulated lens epithelial cells via TGF-β/Smad and Notch1 signaling pathways

Xiaoyu Li^1-3, Honglei Ma⁴

¹Department of Ophthalmology, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, Hubei Province 430061, China; ²Department of Ophthalmology, Affiliated Hospital of Hubei University of Traditional Chinese Medicine, Wuhan, Hubei Province 430061, China; ³Department of Ophthalmology, Hubei Province Academy of Traditional Chinese Medicine?Wuhan, Hubei Province 430074, China; ⁴Department of Ophthalmology, the Second Hospital of Hebei Medical University, Shijiazhuang City, Hebei Province 050000, China.

For correspondence:- Honglei Ma Email: hl_ma77@163.com Tel:+8613930135392

Accepted: 18 July 2022 Published: 28 August 2022

Citation: Li X, Ma H. Catalpol represses the migration, proliferation and epithelial-mesenchymal transition of TGF-β2-stimulated lens epithelial cells via TGF-β/Smad and Notch1 signaling pathways. Trop J Pharm Res 2022; 21(8):1589-1593 doi: 10.4314/tjpr.v21i8.2

© 2022 The authors.
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Abstract

Purpose: To investigate the role of catalpol in posterior capsule opacification (PCO).

Methods: Human lens epithelial cells (SRA01/04) were treated with TGF-β2 or co-treated with TGF-β2 and different concentrations of catalpol. Cell migration and viability were assessed via wound healing and CCK8, respectively. Epithelial-mesenchymal transition and the underlying mechanism of action were evaluated using western blot.

Results: Treatment with TGF-β2 significantly increased cell viability and promoted the migration of SRA01/04 (p < 0.001). However, catalpol significantly reduced cell viability and repressed the migration of TGF-β2-stimulated SRA01/04 (p < 0.001). Moreover, TGF-β2-stimulated increases in fibronectin, α-smooth muscle actin (α-SMA), snail and vimentin. Decreases of E-cadherin and connexin-43 in SRA01/04 were reversed by catalpol. Moreover, TGF-β2-stimulated the up-regulation of p-smad2/3, while SRA01/04 was down-regulated by catalpol, but attenuated TGF-β2-stimulated increases in Notch1 and Jagged1 in SRA01/04.

Conclusion: Catalpol inhibits TGF-β2-stimulated migration, proliferation and epithelial-mesenchymal transition of SRA01/04 through the inactivation of TGF-β/Smad and Notch1 signaling. Catalpol might be a novel preventive agent for PCO. However, the effect of catalpol on animal models of PCO should be investigated further.

Keywords: Catalpol, TGF-?2, Lens epithelial cells migration, Proliferation, Epithelial-mesenchymal transition