Naringenin prevents pregnancy‐induced hypertension via suppression of JAK/STAT3 signalling pathway in mice

Abstract

Pregnancy-induced hypertension (PIH) is also called gestational hypertension, which is developed in the late pregnancy. It is estimated that 7%-10% of pregnancies are affected by PIH which compromises the normal pregnancy process. 1 PIH has been considered as the major cause of perinatal and maternal mortality. 2 The pathogenic mechanisms of PIH remain unclear. One of the major hallmarks in PIH is endothelial dysfunction. Endothelial cells line the internal lumen of the vasculature and participate in

Relationship between Effect of Dietary Flavonoid Intake and Risk of Preeclampsia: A Research Study

“…In my opinion, this is first research to comprehensively investigate the impacts of dietary flavonoid intake upon the PE risk in a Chinese population Our study found that high intake levels of dietary flavanones (naringenin) and luteolin were associated with more than 40 % reduced risks of PE, with a significant dose-response trend. This corresponds to these consequences of Duan et al [18] that studied mice with gestational hypertension exposed to 50 mg/kg of naringenin during gestation and found that naringenin could markedly attenuate the systemic inflammatory response by lessening serum levels of the pro-inflammatory cytokines IL-2, IL-6 as well as TNF-α. Qin et al [19] found that naringenin reduced endothelial dysfunction induced by high glucose concentrations among the endothelial cells.…”

“…Qin et al [19] found that naringenin reduced endothelial dysfunction induced by high glucose concentrations among the endothelial cells. Perhaps, Naringenin's protective effect against endothelial dysfunction is partly regulated through down-regulating the apoptosis and oxygenated stress by means of Phosphorylation of Protein Kinase C βII (PKCβII)-associated caspase-3 and Nitric Oxide (NO)/Reactive Oxygen Species (ROS) pathway among endothelial cells [18][19][20] . Previous studies have indicated that hesperetin treatment can significantly lessen these expressions of Matrix Metalloproteinase (MMP) and MMP-9, while MMPs have been shown to be related to angiogenesis and metastasis [21,22] .…”

NANOG regulate the JAK/STAT3 pathway to promote trophoblast cell migration and epithelial‐mesenchymal transition (EMT) in hypertensive disorders of pregnancy (HDP) through protein interaction with CDK1

“…The activation of the JAK2/STAT3 signaling pathway is closely related to the progress of HDP. Using inhibition of the JAK2/STAT3 signaling pathway (AG490) 36 or Naringenin 37 can reduce the secretory ability of vascular endothelium cells through inhibition activation of the JAK2/STAT3 signaling pathway, and further improve HDP. Then, in this study, we found that NANOG could regulate the expression of STAT3, inhibit JAK2/STAT3 signaling pathway, and promote trophoblast cell proliferation, migration and EMT.…”

Naringenin – a potential nephroprotective agent for diabetic kidney disease: A comprehensive review of scientific evidence

“…Also, the serum levels of IL-2, IL-6, and TNF-α were decreased, while IL-10 was increased. Interestingly, naringenin inhibited Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling by suppressing Src homology region 2 (SH-2) domain-containing phosphatase 1 (SHP-1) expression in vascular endothelial cells [65]. Additional protective effects of naringenin on kidney damage may stem from its capacity to regulate vascular tone by influencing enzymes responsible for metabolizing vasoactive substances and hypertensive mechanisms.…”