Objective To investigate the effects of Tianma-Gouteng decoction on neuroinflammation and apoptosis in the acute phase of ICH in mice and its association with the HMGB1/TLR4 signalling pathway. Methods Mice were randomly divided into 4 groups (n=8): the sham group, the model group, the drug group, and the drug combined with glycyrrhizic acid group. The drug quality was controlled by mass spectrometry analysis, while the results were analysed by network pharmacology for targets and pathways. The model was established by intracerebral injection of collagenase VII. The effects of drugs on neurological deficits and brain histopathological damage after ICH were analysed by mNss and HE. TNF-α, IL-6, IL-1β were determined by ELISA assay; the expression levels of bax, bcl2, HMGB1, TLR4, Myd88, TRIF, NF-κB were analysed by WB. Results Compared with the sham group, the neurological deficits and histopathological brain damage were exacerbated in the ICH group, with increased levels of inflammatory expression and apoptosis, and increased expression of pathway-associated proteins. Compared with the ICH group, the neurological deficits and brain histopathological damage in the IT and ITG groups were ameliorated, the levels of inflammatory expression and apoptosis were decreased, and the expression of pathway-associated proteins was reduced to varying degrees.In addition, 509 compounds were obtained by mass spectrometry and network pharmacology, of which 75 components were analysed by pharmacophore analysis and 195 molecules were identified by target prediction for possible interventional effects.Gene Ontology Enrichment Analysis and Kyoto Encyclopedia of Genes and Genomes further verified the relevance of the relevant molecular targets to the inflammatory pathway. Gene Ontology Enrichment Analysis and Kyoto Encyclopedia of Genes and Genomes Enrichment Analysis further verified the correlation between the relevant molecular targets and inflammation, HMGB1/TLR4 pathway. Conclusion Tianma-Gouteng decoction alleviated neurological deficits and brain histopathological damage, and reduced neuroinflammatory expression and apoptosis levels after ICH, with the possible molecular mechanism being inhibition of HMGB1/TLR4 pathway expressio.