Objective: To preliminarily explore the therapeutic effect and possible regulatory mechanism of heme oxygenase inducer hemin (Hemin) in rats with pregnancy-induced hypertension (HDCP).
Methods: Eighteen pregnant SD rats were randomly divided into 3 groups (6 rats/group) on the 12th day of pregnancy: HDCP model group, Hemin intervention group, and normal pregnancy group. The HDCP model group and the Hemin intervention group were given nitroso-L-arginine methyl ester (80 mg/kg) by gavage for 7 consecutive days from the 14th day of pregnancy to establish the HDCP model. The normal pregnancy group was given the same amount of normal saline by gavage. The Hemin intervention group was given intraperitoneal injection of Hemin (30 mg/kg) every afternoon from the 16th day of pregnancy. The activity of heme oxygenase (HO) and the level of carboxyhemoglobin (COHb) in placental tissue of each group were determined by spectrophotometry. -1), vascular endothelial growth factor (VEGF) levels.
Results: On the 20th day of pregnancy, the blood pressure and 24 h urine protein of the HDCP model group were significantly higher than those in the normal pregnancy group and the Hemin intervention group (P<0.05), while the HO activity and COHb content were significantly lower than those in the normal pregnancy group and the Hemin intervention group. (P<0.05), blood pressure and 24 h urine protein in the Hemin intervention group were higher than those in the normal group (P<0.05), while HO activity and COHb content were lower than those in the normal group (P<0.05). The level of 1 was significantly higher than that in the normal pregnancy group and the Hemin intervention group (P<0.05), while the level of VEGF in the placenta tissue was significantly lower than that in the normal pregnancy group and the Hemin intervention group (P<0.05). The level was higher than that of the normal group (P<0.05), while the level of VEGF was lower than that of the normal group (P<0.05).
Conclusion: Hemin can reduce blood pressure and urinary protein in pregnant mice with gestational hypertension, and its possible mechanism is to increase the activity of HO in placental tissue, increase the metabolite CO, reduce sFIt-1 in placental tissue, and increase the level of VEGF. regulating effect.