Objective To explore the effect of minimally invasive puncture assisted by 3D slicer software combined with atorvastatin on hypertensive cerebral hemorrhage and its effect on postoperative serum interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) levels, and to provide a basis for clinical. Methods A total of 160 patients with hypertensive cerebral hemorrhage from January 2015 to June 2019 in the Department of Neurosurgery, Taizhou Chinese Medicine Hospital, were selected, and were randomly divided into the control group (group C) and the atorvastatin group (group A). The patients in both groups underwent 3D slicer software-assisted minimally invasive puncture. The patients in group A were given atorvastatin for 28 days from the first day after surgery. The state of consciousness were evaluated using the conscious state GCS score. The hematoma clearance rate was calculated. The mRS was used to evaluate the functional recovery of the two groups of patients. The serum IL-6 and TNF-α levels before and after surgery were determined by enzyme-linked immunosorbent assay (ELISA). Results Comparison of postoperative pulmonary infection rate, venous thrombosis rate, urinary tract infection rate and incidence of gastrointestinal bleeding in the two groups, after test, the postoperative pulmonary infection rate in group A was lower than that of group C (P < 0.05).the venous thrombosis rate, urinary tract infection rate and incidence of gastrointestinal bleeding were not statistically significant between two groups(P > 0.05). After surgery, the GCS scores and serum IL-6 and TNF-α levels in the two groups were higher than those before surgery (P < 0.05); the GCS score of group A was higher than that of group C (P < 0.05); the levels of serum IL-6 and TNF-α in group A were lower than those in group C (P < 0.05); the mRS score of group A was lower than that of group C (P < 0.05). Conclusion Minimally invasive puncture combined with atorvastatin can improve the treatment efficacy of hypertensive intracerebral hemorrhage, and its mechanism may be related to the inhibition of postoperative inflammatory response by atorvastatin.