Abstract |
Chlorogenic acid (CGA) is a widely applied traditional Chinese medicine ingredient which can be used for the treatment of osteoporosis. In this experiment, we investigated the potential therapeutic effect of chlorogenic acid on thiram-induced tibial dyschondroplasia (TD) and explored the underlying mechanisms that have been rarely mentioned by others yet. Performance indicator analysis and tibial parameter analysis showed that CGA exhibited a definite positive effect on thiram-induced TD chickens. In order to further explore the mechanisms underlying the positive actions of CGA, apoptotic, autophagic genes and MMPs involved in matrix mineralization of growth plate were evaluated in this study. The results showed that CGA decreased the expression of pro-apoptotic genes caspases-3 and caspases-9, leading to the reduction of apoptotic cells accumulated in growth plate. In addition, CGA also increased the level of BECN1, an important gene involved in autophagy, which benefits the survival of abnormal cells. Furthermore, CGA also increased the expression of MMP-9, MMP-10, and MMP-13, which can directly affect the ossification of bones. Altogether, these results demonstrate that CGA possesses a positive therapeutic effect on thiram-induced TD via modulating the expression of caspases and BECN1 and regulating the degradation of ECM (extracellular matrix).
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Authors | Jialu Zhang, Shucheng Huang, Xiaole Tong, Lihong Zhang, Xiong Jiang, Hui Zhang, Khalid Mehmood, Jiakui Li |
Journal | International journal of molecular sciences
(Int J Mol Sci)
Vol. 20
Issue 13
(Jun 28 2019)
ISSN: 1422-0067 [Electronic] Switzerland |
PMID | 31261680
(Publication Type: Journal Article)
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Chemical References |
- Beclin-1
- Thiram
- Chlorogenic Acid
- Caspases
- Matrix Metalloproteinases
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Topics |
- Animals
- Apoptosis
- Autophagy
- Beclin-1
(genetics, metabolism)
- Caspases
(genetics, metabolism)
- Chickens
- Chlorogenic Acid
(pharmacology, therapeutic use)
- Extracellular Matrix
(drug effects, metabolism)
- Matrix Metalloproteinases
(genetics, metabolism)
- Osteochondrodysplasias
(drug therapy, etiology)
- Thiram
(toxicity)
- Tibia
(drug effects, metabolism, pathology)
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