Effect of ginsenoside Rb1 regulating SIRT1/Nrf2 signaling pathway on oxidative stress injury in gestational diabetes mellitus rats
Objective To investigate the effects of ginsenoside Rb1 regulating silencing information regula-tor 2 related enzyme 1(SIRT1)/nuclear factor E2 related factor 2(Nrf2)signaling pathway on oxidative stress injury in rats with gestational diabetes mellitus(GDM).Methods A total of 39 pregnant SD rats were selected to induce GDM model by intraperitoneal injection of streptozotocin,and a total of 36 rats with suc-cessful modeling were randomly divided into model group(intraperitoneal injection of 10 mL/kg normal sa-line),low-dose ginsenoside Rb1 group(intraperitoneal injection of 1.4 mg/mL ginsenoside Rb1 solution)and high-dose ginsenoside Rb1 group(intraperitoneal injection of 2.8 mg/mL ginsenoside Rb1 solution),ginsen-oside Rb1 high-dose+EX-527 group(intraperitoneally injected 2.8 mg/mL ginsenoside Rb1 and 5.0 mg/mL EX-527 mixed solution),9 patients in each group.Another 9 pregnant SD rats were intraperitoneally injected with the same dose of citrate buffer as the control group.The levels of serum fasting blood glucose(FBG),to-tal cholesterol(TC),high density lipoprotein cholesterol(HDL-C),low density lipoprotein cholesterol(LDL-C)and triglyceride(TG),maternal body weight and fetal rat survival rate in each group were measured.The ratio of placental cells in each group was detected by terminal deoxynucleotidyl transferase-mediated dutp nick-end labeling staining.The levels of malondialdehyde(MDA),glutathione(GSH),superoxide dismutase(SOD)and catalase(CAT)in serum and placental tissues of rats in each group were measured.The expres-sion of SIRT1/Nrf2 pathway associated protein in placental tissue of rats in each group was detected by immu-noblotting.Results Compared with control group,the levels of FBG,TC,LDL-C and TG,maternal body weight,placental cell apoptosis ratio,serum and placental tissue MDA levels in model group were significantly increased(P＜0.05),serum HDL-C,fetal rat survival rate,serum and placental tissue GSH,SOD and CAT levels,placental tissue SIRT,Nrf2 and heme oxygenase-1(HO-1)protein expression levels were significantly decreased(P＜0.05).Compared with model group,FBG,TC,LDL-C and TG levels,maternal body weight,placental cell apoptosis ratio,serum and placental tissue MDA levels in low-dose ginsenoside Rb1 group and high-dose ginsenoside Rb1 group were decreased(P＜0.05),while serum HDL-C,fetal rat survival rate,ser-um and placental tissue GSH,SOD and CAT levels,placental tissue SIRT,Nrf2 and HO-1 protein expression levels were increased(P＜0.05).Compared with low-dose ginsenoside Rb1 group,FBG,TC,LDL-C and TG levels,maternal body weight,placental cell apoptosis ratio,serum and placental tissue MDA levels in high-dose ginsenoside Rb1 group were decreased(P＜0.05),and serum HDL-C,fetal rat survival rate,serum and pla-cental tissue GSH,SOD and CAT levels,placental tissue SIRT,Nrf2 and HO-1 protein expression levels were increased(P＜0.05).Compared with high-dose ginsenoside Rb1 group,the levels of serum FBG,TC,LDL-C and TG,maternal body weight,placental cell apoptosis ratio,serum and placental tissue MDA levels in ginsen-oside Rb1 high-dose+EX-527 group were significantly increased(P＜0.05),and serum HDL-C,fetal rat sur-vival rate,serum and placental tissue GSH,SOD and CAT levels,placental tissue SIRT,Nrf2 and HO-1 pro-tein expression levels were significantly decreased(P＜0.05).Conclusion The intervention effect of high-dose ginsenoside Rb1 is better than that of low-dose ginsenoside Rb1,and EX-527 can weaken the intervention effect of high-dose ginsenoside Rb1 on GDM rats.Ginsenoside Rb1 may enhance antioxidant function and im-prove glucose and lipid metabolism of GDM rats by activating SIRT1/Nrf2 signaling pathway,thereby inhibi-ting placental apoptosis,improving maternal obesity and adverse pregnancy outcomes and finally alleviating oxidative stress injury.
ginsenoside Rb1silence information regulatory factor 2-related enzyme 1/nuclear factor E2 related factor 2 signaling pathwaygestational diabetes mellitusratglycolipid metabolismapopto-sisoxidative stress
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