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Abstract Title:

Emodin induces apoptosis and autophagy of fibroblasts obtained from patient with ankylosing spondylitis.

Abstract Source:

Drug Des Devel Ther. 2019 ;13:601-609. Epub 2019 Feb 11. PMID: 30809091

Abstract Author(s):

Cong Ma, Bo Wen, Qin Zhang, Pei-Pei Shao, Wen Gu, Kun Qu, Yang Shi, Bei Wang

Article Affiliation:

Cong Ma

Abstract:

Background: Ankylosing spondylitis (AS) is a type of rheumatoid disease, which has been reported to be associated with the excessive proliferation of fibroblasts recently. Emodin, a single component from a traditional Chinese medicine, exerts anti-inflammation and antirheumatic arthritis activities. However, could emodin be used to treat AS remains unclear? Thus, this study aimed to investigate the effect of emodin on AS.

Methods: Fibroblasts obtained from patients with AS were used in the current study. In addition, multiple cellular and molecular biology techniques such as Cell Counting Kit-8, Western blotting, flow cytometry, monodansylcadaverine staining, and immunofluorescence assay were applied as well.

Results: Emodin-induced apoptosis of fibroblasts obtained from patient with AS via increasing active caspase-9, active caspase-3, and Bax levels and downregulating Bcl-2. Meanwhile, emodin enhanced autophagy in fibroblasts via upregulation of the expression of Atg12, Atg5, and Beclin 1, which was further confirmed by monodansylcadaverine staining. As expected, autophagy inhibitor 3-methyladenine (3MA) completely reversed emodin-induced autophagy in fibroblasts. Moreover, 3MA significantly increased emodin-induced apoptosis of fibroblasts obtained from patient with AS by increasing the levels ofγH2AX, active caspase-9, active caspase-3, and cleaved poly ADP-ribose polymerase.

Conclusion: Our results indicated that emodin effectively induced apoptosis and autophagy of fibroblasts obtained from patient with AS. In addition, suppression of autophagy enhanced emodin-induced apoptosis in fibroblasts. Therefore, we proposed that combination of emodin with autophagy inhibitor might be a potent strategy for improving the symptoms of AS in the future.

Study Type : Human In Vitro
Additional Links
Pharmacological Actions : Apoptotic : CK(2958) : AC(2075)

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Sayer Ji
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