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Title:
Study on Luteolin Inhibiting the Trabecular Meshwork Fibrosis
Authors:  Jing Yang, M.M., Yiyu Shi, B.S., Haibo Chen, Ph.D., Mingbing Zeng, Ph.D., Jun Yang, M.M., and Xingwu Zhong, Ph.D.
  Objective: To explore the inhibitory effect of luteolin on glaucoma-related cytokines and trabecular meshwork fibrosis, and to provide new ideas for clinical treatment of glaucoma.
Study Design:
Human primary trabecular meshwork cells were cultured. Dexamethasone was applied to induce human trabecular meshwork cells to fibrosis. After luteolin intervention, transforming growth factor–beta 2 (TGF-β2), SFRP1 cytokines, and FN, COL-IV, LN, and other extracellular matrix protein expression levels were all measured to evaluate the inhibitory effect of luteolin on glaucoma-related cytokines and trabecular meshwork fibrosis. TGF-β2 overexpression adenovirus vector was used to make a high intraocular pressure mouse model, in which the luteolin intervention was explored.
Results:
Dexamethasone can increase the expression levels of extracellular matrix proteins such as FN, COL-IV, and LN, as well as cytokines such as TGF-β2 and SFRP1 in human trabecular meshwork cells. After luteolin intervention, the expression levels of the extracellular matrix protein and glaucoma-related cytokines were significantly reduced. Luteolin can significantly reduce the intraocular pressure in mice of a high intraocular pressure model established by adenovirus vector with TGF-β2 overexpression.
Conclusion:
Luteolin can inhibit trabecular meshwork fibrosis and reduce the expression of glaucoma-related cytokines. Luteolin has the effect of reducing intraocular pressure in animal models of high intraocular pressure. This study provides an experimental basis for the treatment of glaucoma.
Keywords:  fibrosis, intraocular pressure, luteolin, trabecular meshwork cells
   
   
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