BACKGROUND: Wogonin is a flavonoid extracted from the root of Scutellaria baicalensis. Previous studies have shown that baicalein has protective effects against cerebral ischemia-reperfusion injury, and can also reduce blood sugar and complications in diabetic mice, but its role and mechanism in diabetic cerebral infarction remain unclear. OBJECTIVE: To explore the effect of wogonin on nerve injury in rats with diabetic cerebral infarction and its mechanism. METHODS: Sprague-Dawley rats were randomly divided into six groups: control group, model group, low-dose wogonin group, medium-dose wogonin group, high-dose wogonin group, and high-dose wogonin+ Ras homolog gene family member A (RhoA) activator group. Except for the control group, the other rats were established with diabetes and cerebral ischemia models using intraperitoneal injection of streptozotocin and middle cerebral artery occlusion. Low, medium- and high-dose wogonin groups were intragastrically given 10, 20, 40 mg/kg wogonin, respectively; high-dose wogonin+RhoA activator group was intragastrically given 40 mg/kg wogonin and intraperitoneally injected 10 mg/kg lysophosphatidic acid; control group and model group were given the same amount of normal saline once a day for 7 consecutive days. Rats in each group were evaluated for neurological deficits and their blood glucose levels were measured after the last dose. TTC staining was applied to detect the volume of cerebral infarction. Hematoxylin-eosin staining was applied to observe pathological changes in brain tissue. ELISA kit was applied to detect tumor necrosis factor-α, interleukin-6, malondialdehyde, and superoxide dismutase levels in brain tissue. Western blot was applied to detect the protein expression of RhoA and Rho-associated protein kinase (ROCK) 2 in brain tissue. RESULTS AND CONCLUSION: Compared with the control group, the neuronal structure of rats in the model group was severely damaged, with cell necrosis and degeneration, the neurological deficit score, blood glucose level, and infarct volume were significantly elevated (P < 0.05), the levels of tumor necrosis factor-α, interleukin-6, and malondialdehyde, and the protein expression of RhoA and ROCK2 in brain tissue were significantly increased (P<0.05), and the superoxide dismutase level was decreased (P<0.05). Compared with the model group, the low-, medium-, and high-dose wogonin groups showed improved neuronal damage, reduced cell degeneration and necrosis, a significant reduction in neurological deficit score, blood glucose level, infarct volume, and the levels of tumor necrosis factor-α, interleukin-6, and malondialdehyde, and the protein expression of RhoA and ROCK2 in brain tissue, and an increase in the superoxide dismutase level (P<0.05). Compared with the high-dose wogonin group, the high-dose wogonin+RhoA activator group significantly weakened the improvement in the above indexes of rats with diabetic cerebral infarction (P<0.05). To conclude, wogonin can improve the blood glucose level in rats with diabetic cerebral infarction, reduce cerebral infarction and nerve injury, and its mechanism may be related to the inhibition of RhoA/ROCK signaling pathway. [ABSTRACT FROM AUTHOR]