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 (p < .05). The SBP, DBP, and 24‐hr urine protein levels were significantly improved (p < .05) in vivo and in vitro. The positive apoptosis cells and apoptosis rate were significantly increased with MyD88 and NF‐κB (p65) proteins upregulation (p < .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 (p < .05). Gastrodin improves PE‐induced cell apoptosis and pathology changed via MyD88/NF‐κB pathway in vitro and in vivo study.