FK228 Ameliorates the Liver Toxicity and Oxidative Stress on Thiram-Induced Tibial Dyschondroplasia in Chicken

Tibial dyschondroplasia (TD) is a disorder of rapidly growing avian species characterized by enlarge avascular growth plate with lesions in proximal tibiotarsal bone. The aim of present study was to investigate the antioxidant capacity of FK228 and role of vascular endothelial growth factor (VEGF) and Flk-1 genes in thiram induced TD. One hundred and fifty broiler chicks were equally divided into 3 groups: control; thiram fed; and FK228 treatment group. Expressions of VEGF and Flk-1 genes were analyzed by real-time quantitative polymerase chain reaction (RT-qPCR) on day 10 and 14 post-hatch. Liver damage caused by thiram was analyzed through levels of antioxidant enzymes (SOD; GSH-Px) and serum biomarkers and the protective effects of the medicine was assessed through these values. Results showed that VEGF mRNA levels were significantly (P<0.05) up-regulated; however, the Flk-1 receptor levels were down-regulated in TD-affected birds significantly (P< 0.05) as compared with the control group. Furthermore, thiram induction also increased the levels of AST, ALT and MDA contents in liver, whereas decreased the antioxidant enzymes (SOD; GSH-Px) and ALP values in thiram group, while these values were found close to normal range in FK228 group as compared to control group in response to FK228 treatment. In conclusion, VEGF and Flk-1 genes play an important role in the formation of avascular growth plate, whereas FK228 can heal lameness and avascularized growth plate in broiler chickens. So, it is effectual through rectifying the oxidative imbalance and liver damage.

Automated summary

This study aimed to investigate the antioxidant capacity of FK228 and the role of VEGF and Flk-1 genes in thiram-induced TD. The results showed that VEGF mRNA levels were up-regulated while Flk-1 receptor levels were down-regulated in TD-affected birds. Additionally, FK228 treatment improved liver damage caused by thiram.