| 杨元晨,李娟,王丽娟,等.黄芪多糖对早产大鼠并发绒毛膜羊膜炎的改善及对胎鼠肺功能的影响[J].安徽医药,2024,28(6):1097-1102. |
| 黄芪多糖对早产大鼠并发绒毛膜羊膜炎的改善及对胎鼠肺功能的影响 |
| Effects of Astragalus polysaccharides on the improvement of chorioamniotic inflammation in premature rats and lung function in fetal rats |
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| DOI：10.3969/j.issn.1009-6469.2024.06.008 |
| 中文关键词: 黄芪 多糖类 早产儿 绒毛膜羊膜炎 肺功能 丝裂原活化蛋白激酶 /胞外信号调节激酶通路 大鼠， Sprague-Dawley |
| 英文关键词: Astragalus membranaceus Polysaccharides Premature infants Chorioamnionitis Lung function MAPK/ERK pathway Rats, Sprague-Dawley |
| 基金项目:2013年度南京市医学科技发展项目( YKK13183) |
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| 中文摘要: |
| 目的观察黄芪多糖对早产大鼠并发绒毛膜羊膜炎( CA)的改善及对胎鼠肺功能的影响，并探讨可能机制。方法于 2021年 10月至 2022年 4月取 40只 SD孕鼠以随机数字表法分为假手术组、 CA组、黄芪多糖组、联合组，各 10只。 CA组、黄芪多糖组、联合组孕鼠羊膜囊均注射脂多糖生理盐水溶液 40 μL(含脂多糖 1 μg)，假手术组注射生理盐水 40 μL。联合组孕鼠腹腔注射黄芪多糖( 800 mg/kg)，尾静脉注射表皮生长因子［丝裂原活化蛋白激酶( MAPK)/胞外信号调节激酶( ERK)通路激动剂(EGF)］(10 μg/kg)；黄芪多糖组腹腔注射黄芪多糖( 800 mg/kg)1h后尾静脉注射等体积生理盐水；假手术组、 CA组腹腔、尾静脉均注射等体积生理盐水。每日 1次，干预 2d。酶联免疫吸附测，定( ELISA)检测胎盘组织肿瘤坏死因子 α(TNF-α)、白细胞介素-6(IL-6)水平；肺功能检测仪检测胎鼠肺功能；苏木精 -伊红(HE)染色检测胎肺组织病理变化；逆转录 -聚合酶链反应(RT-qPCR)法检测胎肺组织 p38 MAPK、ERK1/2 mRNA相对表达量；蛋白质印迹法检测胎肺组织 p38 MAPK、磷酸化 p38 MAPK(p-p38 MAPK)、 ERK1/2、磷酸化 ERK1/2(p-ERK1/2)蛋白表达量。结果与 CA组比较，黄芪多糖组胎盘组织 TNF-α［(192.73±23.67) μg/L比( 371.05±45.33)μg/L］、 IL-6水平［( 241.55±19.94)μg/L比( 512.48±43.16)μg/L］，吸气峰值流速( PIF)［( 96.39±9.78)mL/s比( 126.45±15.41)mL/s］胎肺组织 p-p38 MAPK/p38 MAPK(0.15±0.02比 0.87±0.12)、 p-ERK1/2/ERK1/2(0.22±0.03比 0.81±0.09)降低，每分钟通气量( MV)［，(0.20±0.02)mL比( 0.16±0.02)mL］、潮气量［( 4.14±0.46)mL比( 3.51±0.3)mL］、呼气峰值流速( PEF)［(214.28±23.81)mL/s比( 180.45±16.93)mL/s］升高( P<0.05)；与黄芪多糖组比较，联合组胎胎盘组织 TNF-α［(293.24±27.35)μg/ L比( 192.73±23.67)μg/L］、 IL-6水平［(367.13±32.88)μg/L比( 241.55±19.94)μg/L］，PIF［(119.06±11.81)mL/s比( 96.39±9.78)mL/s］，胎肺组织 p-p38 MAPK/p38 MAPK(0.43±0.06比 0.15±0.02)、 p-ERK1/2/ERK1/2(0.34±0.04比 0.22±0.03)升高， MV［( 0.18±0.02)mL比( 0.20±0.02)mL］、潮气量［(3.74±0.32)mL比( 4.14±0.46)mL］、 PEF降低［(192.03±21.81)mL/s比( 214.28±23.81)mL/s］(P<0.05)，组间胎肺组织 p38 MAPK、ERK1/2 mRNA相对表达量差异无统计学意义( P>0.05)。结论黄芪多糖可抑制 CA孕鼠炎症反应，提升早产胎鼠肺功能，并促进肺发育，推测其作用机制可能与抑制 MAPK/ERK信号通路有关。 |
| 英文摘要: |
| Objective To observe the effect of Astragalus polysaccharide on the improvement of chorioamniotic inflammation in premature rats and lung function in fetal rats, and to explore the possible mechanism.Methods From October 2021 to April 2022, fortypregnant SD rats were randomly divided into sham operation group, CA group, astragalus polysaccharide group and combined groupwith 10 rats each. Pregnant mice in CA group, Astragalus polysaccharide group and combined group were injected with lipopolysaccharide saline solution of 40 μL (containing lipopolysaccharide 1 μg) in amniotic sac, and sham operation group was injected with normalsaline solution of 40 μL. Pregnant rats in the combined group received intraperitoneal injection of astragalus polysaccharide (800 mg/kg) and tail vein injection of epidermal growth factor [mitogen activated protein kinase (MAPK)/extracellular signal regulated kinase(ERK) pathway agonist (EGF)] (10 μg/kg). In the astragalus polysaccharide group, astragalus polysaccharide (800 mg/kg) was intraperitoneally injected, and the same volume of normal saline was injected into the tail vein 1 hour later. The sham operation group and CAgroup were injected with the same volume of normal saline into the abdominal cavity and tail vein, once a day for 2 days. Placental inflammatory factor and tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) levels were detected by ELISA. The lung function of fetalrats was detected by pulmonary function detector. HE staining was used to detect the pathological changes of fetal lung tissue. The relative expression of p38 MAPK and ERK1/2 mRNA in fetal lung tissue was detected by RT-qPCR. The expression of p38 MAPK, p-p38 MAPK, ERK1/2, p-ERK1/2 protein in fetal lung tissue was detected by Western blotting.Results Compared with CA group, the levels of TNF-α [(192.73±23.67) μg/L vs. (371.05±45.33) μg/L] and IL-6 [(241.55±19.94) μg/L vs. (512.48±43.16) μg/L] in the placental tis sue, peak inspiratory flow (PIF) [(96.39±9.78) mL/s vs. (126.45±15.41) mL/s], p-p38 MAPK/p38 MAPK (0.15±0.02 vs. 0.87±0.12), pERK1/2/ERK1/2 (0.22±0.03 vs. 0.81±0.09) in the fetal lung tissue were decreased,of which the minute ventilation (MV) [(0.20±0.02) mL vs. (0.16±0.02) mL], tidal volume (TV) [(4.14±0.46) mL vs. (3.51±0.3) mL], and peak expiratory flow (PEF) [(214.28±23.81) mL/s vs. (180.45±16.93) mL/s]were increased in the astragalus polysaccharide group (P<0.05). Compared with the astragalus polysaccharide group, the levels of TNF-α [(293.24±27.35) μg/L vs. (192.73±23.67) μg/L] and IL-6 [(367.13±32.88) μg/L vs. (241.55±19.94) μg/L] in the placental tissue, peak inspiratory flow (PIF) [(119.06±11.81) mL/s vs. (96.39±9.78) mL/s], p-p38 MAPK/p38 MAPK (0.43±0.06 vs. 0.15±0.02), p-ERK1/2/ERK1/2 (0.34±0.04 vs. 0.22±0.03) in the fetal lung tissue were increased, of which the minute ventilation (MV) [(0.18±0.02) mL vs. (0.20±0.02) mL], tidal volume (TV) [(3.74±0.32) mL vs. (4.14±0.46) mL], and peak expiratory flow (PEF) [(192.03± 21.81) mL/s vs. (214.28±23.81) mL/s] were decreased in the combined group (P<0.05). There was no significant difference in the relative expression of p38 MAPK and ERK1/2 mRNA in fetal lung between groups (P>0.05).Conclusions Astragalus polysaccharide caninhibit the inflammatory response of CA pregnant mice, improve the lung function of premature fetal mice, and promote lung development. It is speculated that its mechanism may be related to the inhibition of MAPK/ERK signaling pathway. |
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