Objective To investigate the effects of ropivacaine on oxidative stress, inflammation and the pathway of phosphatidylinositol 3 kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) in preeclampsia rats. Methods According to the random number table method, eighty‑four pregnant rats at d 12 were randomly divided into control group, model group, low‑dose ropivacaine group (intrathecal injection of 40 μl 0.25% ropivacaine), high‑dose ropivacaine group (intrathecal injection of 40 μl 0.75% ropivacaine),　magnesium sulfate group (gavage of 30 mg/kg magnesium sulfate), PI3K inhibitor (BKM120) group (gavage of 40 mg/kg BKM120), and high‑dose ropivacaine+BKM120 group (intrathecal injection of 40 μl 0.75% ropivacaine and gavage of 40 mg/kg BKM120), with 12 rats in each group. Except for the control group, rats in all other groups were injected intraperitoneally with L‑nitroarginine methyl ester (L‑NAME) once a day from day 13 to 19 of pregnancy to construct a preeclampsia rat model. During day 13 to 19 of pregnancy, rats in each group were treated with drugs once a day via intrathecal and gastric administration, respectively. The diastolic and systolic blood pressure of rats in each group, as well as the 24 h urine protein content were measured. Hematoxylin eosin (HE) staining was used to detect pathological changes in placental tissue of rats in each group while the Enzyme linked immunosorbent assay (ELISA) was used to detect the levels of interleukin‑6 (IL‑6), IL‑1 β, tumor necrosis factor‑α (TNF‑α), superoxide dismutase (SOD), glutathione peroxidase (GSH px) activity, and malondialdehyde (MDA) content in rat placental tissue. The Western blot was used to detect the expression of phosphorylated PI3K (p‑PI3K), phosphorylated Akt (p‑Akt), and phosphorylated mTOR (p‑mTOR) proteins in rat placental tissue. Results Compared to the control group, model group rats had disordered arrangement of trophoblast cells and a large number of inflammatory cell infiltration. increased diastolic blood pressure, systolic blood pressure, 24 h urine protein content, IL‑6 level, IL‑1β level, TNF‑α level, and MDA content, while SOD, GSH‑px activity, and decreased p‑PI3K, p‑Akt, and p‑mTOR protein expression levels (all P<0.05). Compared with the model group, the low‑dose ropivacaine group, high‑dose ropivacaine group, and magnesium sulfate group of rats had lower levels of disorder in the arrangement of trophoblast cells in placental tissue, less infiltration of inflammatory cells, and lower levels of diastolic blood pressure, systolic blood pressure, 24‑hour urinary protein content, IL‑6 level, IL‑1 β level, TNF‑a level, and MDA content (all P<0.05). The activities of SOD, GSH‑px, as well as the levels of p‑PI3K, p‑Akt, and p‑mTOR were higher (all P<0.05). The trend of changes in the corresponding indicators of BKM120 group is opposite to the above (all P<0.05). Compared to low‑dose group of ropivacaine, high‑dose group of ropivacaine and the magnesium sulfate group of rats showed a decrease in the degree of disordered arrangement of trophoblast cells, decreased inflammatory cell infiltration, decreased diastolic blood pressure, systolic blood pressure, 24 h urine protein content, IL‑6 level, IL‑1β level, TNF‑α level, and MDA content, increased SOD, GSH‑px activity, and expression of p‑PI3K, p‑Akt, and p‑mTOR proteins (all P<0.05). Compared to high‑dose ropivacaine group, rats of high‑dose ropivacaine+BKM120 group showed an increase in the disordered arrangement of trophoblast cells, significant infiltration of inflammatory cells, increased diastolic blood pressure, systolic blood pressure, 24 h urine protein content, IL‑6 level, IL‑1 β level, TNF‑α level, MDA content, as well as decreased expression of SOD, GSH‑px activity, p‑PI3K, p‑Akt, p‑mTOR proteins (all P<0.05). There was no difference in various indicators between the high‑dose ropivacaine group and the magnesium sulfate group statistical significance (all P>0.05). Conclusion Ropivacaine may inhibit inflammatory reaction and oxidative stress in preeclampsia rats by activating PI3K/Akt/mTOR pathway.