Gastrodin improves preeclampsia-induced cell apoptosis by regulation of TLR4/NF-κB in rats.

To explain gastrodin improved cell apoptosis induced by preeclampsia in vivo and in vitro study. The PE and normal rats were injected with normal saline (Model), low-dose gastrodin (Gas-L), medium-dose gastrodin (Gas-M), and high-dose gastrodin (Gas-H) groups at 50, 100, or 200 mg/kg per day. The rat blood pressure and 24-hr urine protein level were measured at pregnant days 10, 16, and 20. Evaluating pathology by H&E staining, the cell apoptosis by TUNEL, and MyD88 and NF-κB (p65) proteins by IHC assay using H/R to simulate PE cell model. Measuring cell proliferation, apoptosis, and MyD88 and NF-κB (p65) protein expression by MTT, flow cytometry, and WB assay. The SBP, DBP, and 24-hr urine protein levels were significantly different in PE rats ( < .05). The SBP, DBP, and 24-hr urine protein levels were significantly improved ( < .05) in vivo and in vitro. The positive apoptosis cells and apoptosis rate were significantly increased with MyD88 and NF-κB (p65) proteins upregulation ( < .05). The positive apoptosis cells and apoptosis rate were significantly decreased with MyD88 and NF-κB (p65) proteins depressing in gastrodin-treated groups with dose-dependent ( < .05). Gastrodin improves PE-induced cell apoptosis and pathology changed via MyD88/NF-κB pathway in vitro and in vivo study.