ABSTRACT
Rabbit hemorrhagic disease (RHD) is known as rabbit plague and hemorrhagic pneumonia. It is an acute, septic, and highly fatal infectious disease caused by the Lagovirus rabbit hemorrhagic disease virus (RHDV) in the family Caliciviridae that infects wild and domestic rabbits and hares (lagomorphs). At present, RHDV2 has caused huge economic losses to the commercial rabbit trade and led to a decline in the number of wild lagomorphs worldwide. We performed a necropsy and pathological observations on five dead rabbits on a rabbit farm in Tai'an, China. The results were highly similar to the clinical and pathological changes of typical RHD. RHDV2 strain was isolated and identified by RT-PCR, and partial gene sequencing and genetic evolution analysis were carried out. There were significant differences in genetic characteristics and antigenicity between RHDV2 and classical RHDV strain, and the vaccine prepared with the RHDV strain cannot effectively prevent rabbit infection with RHDV2. Therefore, we evaluated the protective efficacy of a novel rabbit hemorrhagic virus baculovirus vector inactivated vaccine (VP60) in clinical application by animal regression experiment. The result showed that VP60 could effectively induce humoral immunity in rabbits. The vaccine itself had no significant effect on the health status of rabbits. This study suggested that the clinical application of VP60 may provide new ideas for preventing the spread of RHD2.
ABSTRACT
BACKGROUND: Fumonisin B1 is categorised as possible carcinogenic to humans which commonly contaminate maize and maize-based products worldwide, FB1, like other environmental pollutants, may activate apoptosis, autophagy, the inflammatory response and oxidative stress. Platycodon grandiflorus polysaccharide (PGPSt) is prepared from a traditional herbal medicine in Asia with tremendous pharmacological activities. However, whether PGPSt could relieve FB1-induced apoptosis has not been elucidated. The study aimed to evaluate the surface morphology of PGPSt and its protective effect on fumonisin B1-induced apoptosis. METHODS: The surface morphology of PGPSt was evaluated by SEM and AFM. Expressions of proteins involved in autophagy and apoptosis were detected by western blot analysis. Western blot, transient transfection, JC-1 and Annexin V-FITC/PI staining, CCK8, Live-cell imaging and autophagy inhibitor were used to observe the effect and explore the mechanism of PGPSt on FB1-induced apoptosis of 3D4/21 cells. RESULTS: PGPSt had triple helix conformation, and had the characteristics of compact, polyporous and agglomerated morphology. PGPSt promoted the expression of LC3-II and Beclin1, reduced the expression of p62, and significantly activated autophagy. PGPSt inhibited the Akt/mTOR signaling pathway at 24 h. Besides, PGPSt increased the expression of Bcl-2 and decreased the expression of Cleaved Caspase-3. PGPSt-mediated autophagy was inhibited by 3-MA, accompanied by the upregulation of Caspase-3 and Cleaved Caspase-3, suggesting that enhanced autophagy inhibited apoptosis. CONCLUSION: PGPSt can activate autophagy, which in turn protects FB1-induced apoptosis. Targeting autophagy may provide a new way to improve the health of humans or animals in FB1 contaminated areas.
