Tibial dyschondroplasia (TD) is an important long bone defect of broiler chickens that disturbs the proximal growth plate and is characterized by non-vascularized cartilage, a distended growth plate and lameness. Celastrol, a medicinal root extract from the plant Tripterygium wilfordii, is reported widely as a well-known heat-shock protein 90 (Hsp90) inhibitor. Recently, Hsp90 inhibition in chondrocyte differentiation and growth-plate vascularization were effective in restoring the morphology of the growth plate. The present study was aimed at investigating Hsp90 inhibition in TD using celastrol. The broiler chicks were divided into three groups; Control; TD induced (40 mg/kg thiram) and celastrol treatment. Hsp90, vascular endothelial growth factor and Flk-1 expressions were evaluated by quantitative real-time polymerase chain reaction and the protein levels of Hsp90 were measured by Western blot analysis. Antioxidant enzymes were determined to assess the liver damage caused by thiram and the protective effects of the medicine were evaluated by levels of serum biomarkers. The expression levels of Hsp90 and vascular endothelial growth factor mRNA transcripts were increased while Flk-1 receptor was decreased in TD-affected chicks. Celastrol therapy inhibited Hsp90 mRNA and protein levels and up-regulated the expressions of receptor Flk-1 in TD-affected tibial growth plates significantly (P< 0.05) in addition to rectifying the damaging effects of thiram on the liver by decreasing the levels of aspartate aminotransferase, alanine aminotransferase and malondialdehyde and correcting the oxidative imbalance. In conclusion, administering celastrol to dyschondroplastic chicks prevented un-vascularized growth plate, lameness and reinstated angiogenesis. Celastrol may be efficacious for the treatment of TD through the inhibition of Hsp90 expression and limiting the liver damage caused by thiram in broiler chickens.

Carotenoids are one of the widespread and ubiquitous lipid-soluble pigments that produce a wide range of colours which are universally found in various plants, microalgae, bacteria and fungi. Recently, interest in using carotenoids as feed ingredients has increased markedly owing to their bioactive and health-promoting properties. In terms of applications, carotenoid-rich products are widely available in the form of food and feed additive, supplements and natural colourants. Carotenoids play a versatile biological role that contributes to therapeutic effects, including anticancer, immunomodulators, anti-inflammatory, antibacterial, antidiabetic and neuroprotective. Dietary supplementation of carotenoids not only improves the production performance and health of poultry birds, but also enhances the quality of egg and meat. Several studies have suggested that the supplementation of plant derived carotenoids revealed numerous health-promoting activities in poultry birds. Carotenoids reduce the oxidative stress in pre-hatched and post-hatched birds through different mechanisms, including quench free radicals, activating antioxidant enzymes and inhibiting the signalling pathways. Use of carotenoids in poultry feed as a part of nutrient that confers bird health and improve product quality. Carotenoids play a critical role for the pigmentation of egg yolk, skin, legs, beak, comb, feather and fat. Birds consumed carotenoid deficient diet resulting hues of their egg yolk or pale coloured skin. Therefore, uniform pigmentation generally indicates the health status and quality of the poultry products. This review aims to gather recent information regarding bioactive properties of carotenoids and highlight pharmaceutical and health beneficial effects of carotenoids for the poultry industry. Additionally, it explores the importance of carotenoids as alternative feed ingredients for poultry to boost the production performance and replace synthetic medicine and nutrients.

Tibial dyschodroplasia (TD) is a most common pathological condition in many avian species that is characterized by failure of growth plate (GP) modeling that leads to the persistence of avascular lesion in the GP. Tetramethylpyrazine (TMP) is widely used to treat neurovascular disorders and pulmonary hypertension, but no report is available about promoting effect of TMP against TD. Therefore, a total of 210 broiler chicks were equally divided into three groups; Control, TD and TMP. During the experiment mortality rate, chicken performance indicators (daily weight, average daily feed intake, average daily weight gain and feed conversion ratio), tibia bone indicators (weight, length, width of tibial and the size of GP) in addition to gene expression of HIF-1α and VEGF were examined. The results showed that TMP administration restore the GP width, increase growth performance, and mitigated the lameness in broiler chickens. The expression of HIF-1α and VEGF increased significantly in TD affected thiram induced chicks. Whereas, TMP treatment down-regulated HIF-1α and VEGF genes and proteins expressions. The present study demonstrates that the TMP plays an important role in angiogenesis during the impairment and recovery of GP in TD via regulation of the HIF-1α/VEGF signaling pathway in chickens.

Radiological therapeutic intervention is feasible and safe in children with BCS. The overall results of stenting/TIPSS are better than with angioplasty; however, long-term results of these interventions need to be evaluated.

Tibial dyschondroplasia (TD) is an avian bone disorder of different aetiologies that may be associated with lameness. The disorder is characterized by focal disruption of endochondral bone formation, with a lack of matrix proteolysis and an accumulation of non-mineralized avascular cartilage. The aim of this study was to determine the expression of extracellular matrix metalloproteinase inducer (EMMPRIN/CD147) in normal, thiram-induced TD lesions and in the process of recovery from TD in broiler chickens. An extracellular matrix (ECM) degrading enzyme, matrix metalloproteinase-9 (MMP-9), was selected to investigate the effects of CD147 in the degradation of ECM. Gene expression was analysed by quantitative real-time polymerase chain reaction and protein levels by immunohistochemistry and western blotting. The birds were divided into three groups: thiram fed; recovery; and controls. Genes encoding CD147 and MMP-9 were down-regulated during the development of the disease, and were up-regulated during recovery. Western blotting also showed lower protein levels of CD147 in TD, which increased during the recovery phase associated with ECM degradation and growth plate repair. The findings of this study suggest that ECM has a crucial role in the occurrence of TD and that CD147 appears to play a pivotal role in matrix proteolysis in the chicken, similar to that in other species.

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