Recovery of Chicken Growth Plate by Heat-Shock Protein 90 Inhibitors Epigallocatechin-3-Gallate and Apigenin in Thiram-Induced Tibial Dyschondroplasia.

Abstract

Tibial dyschondroplasia (TD) is an important tibiotarsal bone disorder characterized by an avascular and nonmineralized growth plate; it is attributed to abnormal differentiation of chondrocytes and causes lameness. Heat-shock protein 90 (Hsp90) is a proangiogenic factor in animal tissues; however, its gene expression increases in cases of chicken TD. The objective of this study was to evaluate the efficacy of epigallocatechin-3-gallate (EGCG) and apigenin in thiram-induced TD birds; these substances were used because of their Hsp90 inhibitory activities. The histologic study of growth plates was carried out with hematoxylin and eosin staining, and the Hsp90 gene expression was examined by reverse transcription quantitative real-time PCR. Results showed that as compared to a control group, TD-affected birds displayed changes in chondrocyte differentiation, with lack of blood vessels, and an increased expression of Hsp90 was observed significantly (P < 0.05). However, on administering the EGCG and apigenin to TD-affected birds, the normal chondrocyte columnar organization was restored with vascularization and decreased Hsp90 expression activity (P < 0.05), which ultimately abrogated the lameness. Our results suggested that Hsp90 is the key factor in the development of TD, and EGCG and apigenin have a novel effect on Hsp90 inhibition properties, thus reducing the lameness and leg deformity in chicken broilers.