Ameliorative Effects of Triptolide against Autophagy and Apoptosis in Thiram Induced Tibial Dyschondroplasia

Tibial dyschondroplasia (TD) is a metabolic bone disease that occurs in fast-growing chickens and can lead to substantial economic damages and compromise the poultry welfare. Triptolide is a traditional Chinese medicine (TCM), which has been broadly used as an anti-inflammatory, and anti-cancerous drug. However, its therapeutic role against tibial dyschondroplasia is under-reported yet. Therefore, the study aimed for investigating the protective effect of triptolide against autophagy and apoptosis in TD affected chickens. Random classification of chickens (n=30) was done into three groups: CON, TD and triptolide treatment group (TP). All chickens were given standard diet until the end of the experiment for 18 days. In this study, tibial bone was collected for analyzing several aspects, serum was collected for biochemical analysis, and microscopic assessment was done by H&E staining. Immunohistochemistry, immunofluorescence, western blotting, and RT-qPCR were used to detect autophagy and apoptosis-related proteins and genes. Observations illustrated that after triptolide treatment, the symptoms of TD group were improved, and tibial parameters were changed. At the same time, the expression of m-TOR and P62 mRNA in TP group showed significant decrease comparing to TD group. Precisely, thiram induced TD was found to be involved in hypertrophic chondrocytes apoptosis and autophagy, and triptolide showed protective effects against TD.

Automated summary

The study aimed to investigate the therapeutic role of Triptolide, a traditional Chinese medicine, against tibial dyschondroplasia (TD) in chickens. The results showed that the symptoms of TD group were improved, and tibial parameters were changed after triptolide treatment. In addition, the expression of m-TOR and P62 mRNA in the triptolide treatment group showed a significant decrease compared to the TD group. Triptolide was found to have protective effects against TD by inhibiting hypertrophic chondrocytes apoptosis and autophagy induced by thiram.