Fig. 1

MPS derived from apoptotic HPCs prevent hepatocarcinogenesis in a primary rat HCC model. A Diagram of the treatment schedule in the rat HCC model. After 6 weeks of oral treatment with diethylnitrosamine (DEN), Sprague Dawley rats were intrasplenically injected with 40 µg of apoHPC-MPs, apoLTC-MPs or apoHep-MPs in 200 µl saline or 200 µl of blank saline. Injections were administered twice every week for 7 weeks. Oral DEN treatment was also continued during this time. After 13 weeks, the rats were sacrificed to observe the development of hepatocellular carcinoma (HCC). B Representative images of rat livers from the indicated groups. Typical tumor nodes are marked by the asterisks. C The maximum tumor volume per liver in the different groups. ****p < 0.0001. D The liver-to-body weight ratio in the different treatment groups. **p < 0.01. E The number of HCC nodules per liver in each group. *p < 0.05, ****p < 0.0001. F The tumor incidence in each group. G Images of H&E-stained liver sections showing the histological structure and inflammatory response in the indicated groups. Black asterisks represent accumulation of inflammatory cells. (H) Body weight curves. The rats were weighed every other week (n = 5 per group). ****p < 0.0001 compared to saline group. (I) Serological analysis of creatine kinase (CK) was performed after the rats were sacrificed. Data are presented as mean ± SD. ns, not statistically significant