Objective To explore the effects of Shenfuhuang Fomula（参附黄方） on inflammation and phagocytosis of macrophages in zebrafish and its mechanism. Methods Transgenic neutrophil fluorescent zebrafish and wild-type AB strain zebrafish were used as experimental subjects to establish a zebrafish inflammation model and a macrophage phagocytosis model

respectively. Mortality and cardiovascular toxicity were applied to screen the medicinal concentration of Shenfuhuang Fomula; neutrophil count was used to evaluate the effect of Shenfuhuang Fomula on zebrafish inflammation model

and indomethacin was set as a control; zebrafish white blood cells interleukin 10（IL-10）

tumor necrosis factor alpha（TNF-α）

inducible nitric oxide synthase（iNOS）

recombinant human arginase 1（ARG1）

interleukin 1β（IL-1β） mRNA expression were detected to evaluate the effect of Shenfuhuang Fomula on the phagocytic function of zebrafish phagocytes. Results The maximum safe concentration of Shenfuhuang Fomula for zebrafish was 10 mg/ml. In this study

the low

medium and high dose concentrations of Shenfuhuang Fomula were 1.1

3.3 and 10 mg/ml

respectively. In the inflammation model

the number of neutrophils in the inflammation site of the model control group was higher than that of the normal control group（P<0.01）; compared with the model control group

in the indomethacin group and in the Shenfuhuang Fomula middle and high dose groups

the number of neutrophils in the inflammation site of zebrafish decreased（P<0.01）; the inflammation subsided in the Shenfuhuang Fomula medium dose group was 44.1%. In the macrophage phagocytic model

compared with the normal control group

the expression of TNF-α and IL-10 mRNA in the Shenfuhuang Fomula medium and high dose groups increased

and the expression of IL-1β mRNA in the Shenfuhuang Fomula high dose group increased

and the expression of ARG1 mRNA decreased（P<0.05 or P<0.01）. Conclusion Shenfuhuang Fomula has a good immune activation effect

and its mechanism may be related to reducing the number of neutrophils and regulating the typing of macrophages.