AIM: To study the protective effect of transient receptor potential vanilic acid subtype 1(TRPV1) agonist capsaicin (CAP) on traumatic blood loss shock rats, and to further explore its possible mechanism by network pharmacology. METHODS: Forty-five SD rats were divided into 5 groups by random number table method: normal group, shock group, lactated Ringer's solution(LR) group, CAP pretreatment (single administration before shock) group, CAP pre-final administration (twice administration before and after shock) group, with 9 rats in each group for survival observation. Then 32 SD rats were divided into 4 groups according to the results of survival experiment: normal group, shock group, LR group, CAP pre-final administration group, with 8 rats in each group for blood pressure, hemodynamics, arterial blood gas, vascular reactivity and hepaticand renal blood flow. At the same time, the potential mechanism of CAP in the treatment of traumatic hemorrhagic shock was investigated by network pharmacology. Furthermore, apply the dataset to validate and analyse the diagnostic value of the hub genes. RESULTS: Rats in shock group died within hours of the completion of the shock model, and the mean survival time was 1.25（0.42,6.21）h. LR resuscitation could improve the survival of rats to some extent. The survival rate and survival time of rats in the CAP pretreatment group were slightly increased as compared with the LR group, while twice administration of CAP before and after shock (CAP pre-final administration) resulted in better outcomes than LR resuscitation alone. Further results indicated that CAP pre-final administration significantly reduced the blood lactic acid level, improved the vasoconstrictive and diastolic reactivity, and increased the liver and kidney blood flow of shock rats as compared with LR group. The improvement of hemodynamics and blood gas indexes in CAP group was slightly higher than LR group,but there was no statistical significance. A total of 37 genes related to CAP anti-traumatic hemorrhage shock were obtained by network pharmacology. KEGG enrichment analysis showed that the Ca ion signaling pathway and Ras signaling pathway were significantly enriched. Validation of the dataset showed that the expression levels of CXCR4, NF-kB1, GFPA and NTF3 hub gene were significantly different in the normal and shock groups, and that CXCR4 has a high diagnostic value for traumatic haemorrhagic shock. CONCLUSIONS: CAP, the TRPV1 agonist, significantly improved vascular function, increased organ blood flow, and corrected the lactic acidosis in rats with traumatic hemorrhagic shock, thus markedly improved the survival outcomes. The mechanism may be related to Ca ion signal pathway and Ras signal pathway. CXCR4, NF-kB1, GFPA and NTF3 may be having an important role in it.