STACHYDRINE PROTECTS NEONATAL RATS FROM HYPOXIC-ISCHEMIC BRAIN INJURY BY REGULATING HDAC ACTIVITY, OXIDATIVE STRESS AND NEURONAL INFLAMMATORY RESPONSE

Objective: To explore the effect and mechanism of artesunate on pain associated with osteoarthritis (OA) and the inflammatory response of chondObjective: The objective was to study the protective effect of stachydrine on hypoxic-ischemic brain injury in neonatal rats by regulating HDAC activity, oxidative stress and neuronal inflammatory response. Methods: Thirty-two newborn SD rats were divided into different groups, namely the control, model group, stachydrine 5mg/ kg, and 10 mg/kg. In addition to the control group, the ischemic and hypoxic brain injury model was established by coronary artery ligation. The infarct area, apoptosis rate of brain tissue, HDAC activity, oxidative stress index, and inflammatory factor levels were observed. Results: The area of cerebral infarction in the cortex of rats in 5 mg/kg and 10 mg/kg dose groups was significantly lower than that in the model group (P < 0.05). The apoptosis rate of brain tissue of stachydrine 5 mg/kg and 10 mg/kg groups was significantly lower than that of the model group (P < 0.05). HDAC activity in brain tissue of stachydrine 5 mg/kg and 10 mg/kg groups was significantly lower than that of the model group (P < 0.05). The expression of acetylated protein H3 and H4 in brain tissue of rats in stachydrine 5mg/kg and 10mg/kg groups were significantly higher than that in the model group (P < 0.05). The levels of SOD, GSH PX, and T-AOC in brain tissue of stachydrine 5 mg/kg and 10 mg/kg groups were significantly higher than those of the model group, and the MDA level was significantly lower than that of the model group (P < 0.05). The levels of TNF-alpha, IL-1 beta, ICAM-1, and VCAM-1 in the 5 mg/kg and 10 mg/kg dose groups were significantly lower than those in the model group (P < 0.05). Conclusion: Stachydrine can improve the damage degree of neonatal rats with hypoxic-ischemic brain injury and has an obvious protective effect. Its mechanism may be achieved by inhibiting HDAC activity, regulating oxidative stress and neuronal inflammatory response.