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Pulmonary hypertension syndrome (PHS) is a poultry disease that causes significant economic losses in broilers. Portal hypertension and liver cirrhosis can cause ascites formation. Disturbance of mitochondrial dynamics causes several diseases; however, its mechanism of action in PHS is not yet fully understood. In this research, 210 broilers were split randomly into two groups: control and PHS. Broilers in the control group were injected with normal saline and those in the PHS group were injected with CM-32 cellulose particles at 20 days of age. Transmission electron microscopy (TEM) was used to assess mitochondrial ultrastructure. Changes in mitochondrial dynamics were measured by immunohistochemical staining, RT-PCR and western blotting. On days 28 and 42, the liver and heart were collected from each group, and the ascites heart index (AHI) and hepatic coefficient were calculated. The results showed that PHS induced hepatocyte damage, reduced mitochondrial size, and increased mitochondrial number. Furthermore, RT-PCR demonstrated the downregulation of Mfn1, Mfn2, and Opa1 mRNA, and the upregulation of Drp1 and Mff mRNA. Protein expression levels detected by immunohistochemistry and western blotting were similar to those obtained by RTPCR. This study showed that mitochondrial fusion in the liver was diminished and mitochondrial fission in the liver was enhanced in PHS broilers. [ABSTRACT FROM AUTHOR]

Tibial dyschondroplasia (TD) is a metabolic bone disease that occurs in fastgrowing 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. [ABSTRACT FROM AUTHOR]

Ascites syndrome (AS) is a common nutritional metabolic disease in broilers that results in major loss to the breeding industry. The occurrence of AS is closely related to the abnormal proliferation of pulmonary artery smooth muscles cells (PASMCs) caused by hypoxia. The transient receptor potential cation channel subfamily C member 6 (TRPC6) is a Ca2+ channel situated on cell membranes, and belongs to the proliferation of PASMCs caused by hypoxia in mammals. However, its role in hypoxic PASMCs in broilers remains unclear. Here, we investigated the effects of TRPC6 on the proliferation and apoptosis of primary chicken PASMCs under hypoxic conditions using an in vitro model. Primary chicken PASMCs were cultured under normoxic or hypoxic conditions (3% O2). The hypoxic cells were treated with 10 μM of SKF 96365 or 50 μM of fluofenamic acid (FFA) to inhibit or activate TRPC6, respectively. Cell viability was detected by CCK-8, intracellular Ca2+ levels, cell cycle and cell apoptosis were assayed by a flow cytometric assay, the mRNA levels of TRPC6 were measured by digital-droplet PCR (ddPCR), the protein levels of TRPC6 were tested by immunoblotting, and the mRNA levels of caspase3 were detected by RT-PCR. Our results revealed that exposing PASMCs to hypoxic conditions for 48h increased cell viability and intracellular Ca2+ levels. Additionally, hypoxic conditions increased the expression of TRPC6 and promoted cell cycle progression, but decreased cell apoptosis and caspase 3 mRNA levels. When the hypoxic PASMCs were treated with SKF 96365, inhibition of TRPC6 and cell proliferation and promotion of apoptosis were observed only in the first 24h of treatment. Treatment with FFA for 24h had the opposite effects. These results suggested that TRPC6-mediated Ca2+ entry contributed to hypoxia-induced PASMCs proliferation and apoptosis resistance, which identified TRPC6 as a possible key target in vascular remodeling in chicken. [ABSTRACT FROM AUTHOR]