Key result
In a rat model of pregnancy-induced hypertension, PPAR-γ activation decreased systolic blood pressure and inhibited ETR expression.
Why the study?
Does PPAR-γ activation improve pregnancy-induced hypertension in rat models?
Does PPAR-γ activation improve pregnancy-induced hypertension in rat models?
In a rat model of pregnancy-induced hypertension, PPAR-γ activation inhibits ETR expression and reduces the effect of ET-1 on vascular contraction, thereby delaying PIH progression.
Answers are grounded in this paper and cite their sources.
May attenuate PIH progression via ETR inhibition in rat models; leaves open translation to human gestational hypertension.
This study aims to investigate the effects of PPAR‐γ on rats with pregnancy‐induced hypertension (PIH) by regulating endothelin receptor (ETR). A total of 60 pregnant Wistar rats were selected, and 50 rats were used to establish endotoxin induced PIH rat models. Rats were equally assigned into PIH‐NS, PIH‐5 mg/kg RM, PIH‐10 mg/kg RM, PIH‐100 mg/kg ETR, and PIH‐200 mg/kg ETR groups, and the rest 10 rats were assigned to a the control group. Reverse transcription quantitative polymerase chain reaction (RT‐qPCR) and Western blotting were used for determining mRNA and protein expressions of PPAR‐γ and ET A R, respectively. Protein expression of ET‐1 was detected by immunohistochemistry. Results show that On the 22nd day of pregnancy, compared with the PIH‐NS group, SBP decreased in other groups, and platelet concentration increased most significantly in the PIH‐10 mg/kg RM and PIH‐200 mg/kg ETR groups. Compared with the control, PIH‐10 mg/kg RM and PIH‐200 mg/kg ETR groups, the increase in the expression of ET‐1 and ET A R was most significant in the PIH‐NS group. Compared with the control and PIH‐10 mg/kg RM groups, expression of PPAR‐γ was lower in the PIH‐NS, PIH‐5 mg/kg RM, PIH‐100 mg/kg ETR, and PIH‐200 mg/kg ETR groups. Compared with the PIH‐NS, PIH‐100 mg/kg ETR and PIH‐200 mg/kg ETR groups, PPAR‐γ expression was significantly higher in the PIH‐5 mg/kg RM group (all P < 0.05). Based on our findings, we conclude that PPAR‐γ activation inhibits ETR expression and reduces the effect of ET‐1 on vascular contraction thereby delaying PIH progression.
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Wu et al. (2017) studied Pregnancy-induced hypertension (n=60). RM (PPAR-γ agonist) and ETR vs. PIH-NS (normal saline) and healthy control was evaluated on Systolic blood pressure, platelet concentration, and expression of PPAR-γ, ETAR, and ET-1 (p=<0.05). In a rat model of pregnancy-induced hypertension, PPAR-γ activation decreased systolic blood pressure and inhibited ETR expression.
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