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

Abstract

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.

Combining curcumin and aspirin ameliorates preeclampsia‐like symptoms by inhibiting the placental TLR4/NF‐κB signaling pathway in rats

“…Placenta inflammation is known to result from TLR4 signaling partially. It has been reported that the activation of the TLR4/NF‐κB pathway has a strong correlation with the development of PE 36 . The activated placental TLR4/NF‐kB pathway, which subsequently induces the secretion of downstream inflammatory cytokines and chemokines, 35 may be another intermediary factor in the cascade reaction of PE.…”

Paeonol alleviates placental inflammation and apoptosis in preeclampsia by inhibiting the JAK2/STAT3 signaling pathway

“…According to previous studies, the crucial function of the activated immune system characterized by an imbalance between anti‐inflammatory and proinflammatory factors in the pathogenesis of PE has been discovered 23 . Substantial evidence has shown that the accelerated apoptosis of trophoblasts and retardant intrauterine growth can be caused by imbalanced concentrations of pro‐ and anti‐inflammatory cytokines in the PE placenta 24 .…”

“…However, injection of SC-39100 reversed these effects (Figure 5E-H According to previous studies, the crucial function of the activated immune system characterized by an imbalance between anti-inflammatory and proinflammatory factors in the pathogenesis of PE has been discovered. 23 Substantial evidence has shown that the accelerated apoptosis of trophoblasts and retardant intrauterine growth can be caused by imbalanced concentrations of pro-and antiinflammatory cytokines in the PE placenta. 24 TNFα, IL-6, and IFN-γ are pivotal proinflammatory cytokines and mediators in the immune system of pregnant women and are overproduced by immune cells of PE patients.…”

The up-regulation of miR-21 by gastrodin to promote the angiogenesis ability of human umbilical vein endothelial cells by activating the signaling pathway of PI3K/Akt

“…This study also confirmed that VEGF can induce the proliferation, migration and tube formation of HUVECs. Besides, from previous studies, it was found that gastrodin can suppress the apoptosis induced by preeclampsia by regulating the TLR4/NF-κB of HTR/SVneo cells [ 19 ]. Liu et al found that gastrodin antagonized the up-regulation of stress signals from the endoplasmic reticulum by activating the Nrf2 pathway, including the expression of GRP78, CHOP, and phosphorylated eIF2α, reducing osteoporosis in rats caused by glucocorticoids [ 20 ].…”