June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Celastrol Suppressed Proliferation of LECs through suppressing the PI3K/Akt, p38MAPK and SAPK/JNK signaling pathways
Author Affiliations & Notes
  • wang liping
    Zhongshan Ophthalmic Center, Guangzhou, China
  • Shan Huang
    Zhongshan Ophthalmic Center, Guangzhou, China
  • Baoxin Chen
    Zhongshan Ophthalmic Center, Guangzhou, China
  • Xiaoxian Lu
    Zhongshan Ophthalmic Center, Guangzhou, China
  • Jieping Chen
    Zhongshan Ophthalmic Center, Guangzhou, China
  • Yizhi Liu
    Zhongshan Ophthalmic Center, Guangzhou, China
  • Footnotes
    Commercial Relationships   wang liping, None; Shan Huang, None; Baoxin Chen, None; Xiaoxian Lu, None; Jieping Chen, None; Yizhi Liu, None
  • Footnotes
    Support  National Natural Science Foundation of China (No.81300749)
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 1705. doi:
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      wang liping, Shan Huang, Baoxin Chen, Xiaoxian Lu, Jieping Chen, Yizhi Liu; Celastrol Suppressed Proliferation of LECs through suppressing the PI3K/Akt, p38MAPK and SAPK/JNK signaling pathways. Invest. Ophthalmol. Vis. Sci. 2017;58(8):1705.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : Celastrol, also known as tripterine, is isolated from the traditional Chinese medicine ‘Thunder of God Vine’. It shows significant activities in the treatment of chronic inflammatory, cancer and diabetic activity. Capsule opacification is the most common complication after cataract surgery. Proliferation of lens epithelial cells (LECs) plays an important role during the pathological process of capsule opacification. It is demonstrated that the phosphatidylinositol-3-kinase(PI3K)/Akt, mitogen-activated protein kinases(MAPKs), p38 pathways and stress-activated protein kinase(SAPK)/JNK have key roles in promoting cell proliferation. The purpose of this study is to investigate the effect and mechanism of celastrol on proliferation of LECs.

Methods : Human lens epithelium cells(SRA01/04) were treated with various concentrations of celastrol(0uM,0.5uM and 1uM). Cell Proliferation Assay was performed to evaluate the dose-dependent effect of celastrol on the proliferation of LECs. Western blot was examined to investigate the mechanism of celastrol on the proliferation of LECs. We detected the protein expression and level of phosphorylation of PI3k/Akt, p38MAPK and SAPK/JNK.

Results : Cell proliferation was attenuated in the 0.5μM group and almost completely inhibited with 1μM after 12 hours (P<0.05). Meanwhile, we found celastrol decreased the level of the phosphorylation of Akt without affecting its total protein levels. Moreover, it decreased the protein levels of p38MAPK and SAPK/JNK. These results suggested that celastrol could inhibit the proliferation of LECs through inactivating PI3k/Akt, p38MAPK and SAPK/JNK signaling pathways.

Conclusions : This study demonstrates that celastrol suppresses the proliferation of LECs. It indicates the possibility that celastrol might be a potential drug in prevention and treatment of Capsule opacification after surgery of caratact.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.

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