Wnt通路对多囊卵巢大鼠子宫内膜降钙素表达的影响
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摘要
目的探讨Wnt通路对多囊卵巢大鼠子宫内膜降钙素表达的影响。方法健康雌性SD大鼠54只随机分为3组:空白组、模型组与Wnt组,每组6只大鼠。Wnt组建立多囊卵巢综合征模型,模型建立后21 d,Wnt组静脉注射阿西替尼30 mg/kg,每3天1次,连续应用7次。模型组也构建多囊卵巢综合征模型,建模后采用PBS注射处理。空白组不建立多囊卵巢综合征模型。记录所有大鼠的血清雌二醇(E2)表达、降钙素表达、肌酸激酶同工酶(CK-MB)和乳酸脱氢酶(LDH)活性等情况。结果模型组与Wnt组大鼠给药第1次、第3次与第7次的血清E2水平显著低于空白组(P <0. 05),Wnt组高于模型组(P <0. 05),不同组别的血清FHS与LH水平对比差异无统计学意义(P> 0. 05)。模型组与Wnt组大鼠给药第1次、第3次与第7次的血清CK-MB和LDH活性都显著高于空白组(P <0. 05),Wnt组显著低于模型组(P <0. 05)。模型组与Wnt组大鼠给药第1次、第3次与第7次的子宫内膜降钙素含量显著低于空白组(P <0. 05),Wnt组高于模型组(P <0. 05)。结论抑制Wnt通路能够抑制多囊卵巢大鼠子宫内膜降钙素表达,从而促使性激素分泌正常,降低CK-MB和LDH活性,改善多囊卵巢综合征症状。
Objective To investigate the effects of Wnt pathway on the expression of calcitonin in endometrium of polycystic ovary rats.Methods 54 healthy SD rats were randomly divided into 3 groups,including blank group,model group and Wnt group,with 18 rats in each group. The Wnt group were established model of polycystic ovary syndrome,21 days after the model were established,the Wnt group were intravenously injected with azithinib 30 mg/kg once every 3 days for 7 consecutive applications. The model group were also established model of polycystic ovary syndrome and given injected with PBS,and the blank group were not established model of polycystic ovary syndrome. The expression of serum E2 expression,calcitonin,CK-MB and LDH activities were recorded. Results The serum E2 levels of in the model group and the Wnt group were significantly lower than those in the blank group( P < 0. 05),and the Wnt group were higher than that of the model group( P <0. 05) at the 1,3 and 7 administrations. There were no significant difference in serum FHS and LH levels compared among the three groups( P> 0. 05). The serum levels of CK-MB and LDH in the model group and Wnt group were significantly higher than those in the blank group( P< 0. 05),and the Wnt group were significantly lower than those of the model group( P < 0. 05) at the 1,3 and 7 administrations. The endometrial calcitonin levels in the model group and the Wnt group were significantly lower than those in the blank group( P < 0. 05),and the Wnt group were higher than the model group( P < 0. 05) at the 1,3 and 7 administrations. Conclusion Inhibition of Wnt pathway can inhibit the expression of calcitonin in endometrium of polycystic ovary rats,which promotes the secretion of sex hormones,reduces the activity of CK-MB and LDH,and improves the symptoms of polycystic ovary syndrome.
Objective To investigate the effects of Wnt pathway on the expression of calcitonin in endometrium of polycystic ovary rats.Methods 54 healthy SD rats were randomly divided into 3 groups,including blank group,model group and Wnt group,with 18 rats in each group. The Wnt group were established model of polycystic ovary syndrome,21 days after the model were established,the Wnt group were intravenously injected with azithinib 30 mg/kg once every 3 days for 7 consecutive applications. The model group were also established model of polycystic ovary syndrome and given injected with PBS,and the blank group were not established model of polycystic ovary syndrome. The expression of serum E2 expression,calcitonin,CK-MB and LDH activities were recorded. Results The serum E2 levels of in the model group and the Wnt group were significantly lower than those in the blank group( P < 0. 05),and the Wnt group were higher than that of the model group( P <0. 05) at the 1,3 and 7 administrations. There were no significant difference in serum FHS and LH levels compared among the three groups( P> 0. 05). The serum levels of CK-MB and LDH in the model group and Wnt group were significantly higher than those in the blank group( P< 0. 05),and the Wnt group were significantly lower than those of the model group( P < 0. 05) at the 1,3 and 7 administrations. The endometrial calcitonin levels in the model group and the Wnt group were significantly lower than those in the blank group( P < 0. 05),and the Wnt group were higher than the model group( P < 0. 05) at the 1,3 and 7 administrations. Conclusion Inhibition of Wnt pathway can inhibit the expression of calcitonin in endometrium of polycystic ovary rats,which promotes the secretion of sex hormones,reduces the activity of CK-MB and LDH,and improves the symptoms of polycystic ovary syndrome.
引文
[1]Aydos A,Gurel A,Oztemur Islakoglu Y,et al.Identification of Polycystic Ovary Syndrome(PCOS)Specific Genes in Cumulus and Mural Granulosa Cells[J].PLo S One,2016,11(12):e0168875.
[2]姜晓琳,张兵,侯海燕,等.二甲双胍联合膈下逐瘀汤对多囊卵巢综合征大鼠炎性因子及性激素水平的影响[J].北京中医药大学学报,2018,41(1):65-70.
[3]Jiao J,Shi B,Wang T,et al.Characterization of long non-coding RNA and messenger RNA profiles in follicular fluid from mature and immature ovarian follicles of healthy women and women with polycystic ovary syndrome[J].Hum Reprod,2018,33(9):1735-1748.
[4]黄威,鲁耀邦,熊桦,等.补肾化瘀方对多囊卵巢综合征大鼠血清25羟基维生素D3、AMH、T、INS及E2的影响[J].湖南中医药大学学报,2018,38(6):650-652.
[5]Mao Z,Fan L,Yu Q,et al.Abnormality of Klotho Signaling Is Involved in Polycystic Ovary Syndrome[J].Reprod Sci,2018,25(3):372-383.
[6]和梦珂,张静,李昕,等.苍附导痰汤对米非司酮诱导PCOS大鼠卵巢形态及雄激素的影响[J].湖南中医药大学学报,2018,38(8):862-865.
[7]Mehdinejadiani S,Amidi F,Mehdizadeh M,et al.The effects of letrozole and clomiphene citrate on ligands expression of Wnt3,Wnt7a,and Wnt8b in proliferative endometrium of women with Polycystic ovarian syndrome[J].Gynecol Endocrinol,2018,34(9):775-780.
[8]Mondal K,Chakraborty P,Kabir S N.Hyperhomocysteinemia and hyperandrogenemia share PCSK9-LDLR pathway to disrupt lipid homeostasis in PCOS[J].Biochem Biophys Res Commun,2018,503(1):8-13.
[9]Mehdinejadiani S,Amidi F,Mehdizadeh M,et al.The effects of letrozole and clomiphene citrate on ligands expression of Wnt3,Wnt7a,and Wnt8b in proliferative endometrium of women with Polycystic ovarian syndrome[J].Gynecol Endocrinol,2018,34(9):775-780.
[10]Qiao GY,Dong BW,Zhu CJ,et al.Deregulation of WNT2/FZD3/beta-catenin pathway compromises the estrogen synthesis in cumulus cells from patients with polycystic ovary syndrome[J].Biochem Biophys Res Commun,2017,493(1):847-854.
[11]Mehdinejadiani S,Amidi F,Mehdizadeh M,et al.Effects of letrozole and clomiphene citrate on Wnt signaling pathway in endometrium of polycystic ovarian syndrome and healthy womendagger[J].Biol Reprod,2019,100(3):641-648.
[12]Wu XQ,Wang YQ,Xu SM,et al.The WNT/beta-catenin signaling pathway may be involved in granulosa cell apoptosis from patients with PCOS in North China[J].J Gynecol Obstet Hum Reprod,2017,46(1):93-99.
[13]何轶然,张治芬,王芳,等.SIRT1、Fox O3a在DHEA诱导多囊卵巢综合征模型大鼠卵巢组织中的表达及意义[J].浙江医学,2018,40(5):429-432,438,后插1.
[14]Jiao J,Shi B,Wang T,et al.Characterization of long non-coding RNA and messenger RNA profiles in follicular fluid from mature and immature ovarian follicles of healthy women and women with polycystic ovary syndrome[J].Hum Reprod,2018,33(9):1735-1748.
[15]Aydos A,Gurel A,Oztemur Islakoglu Y,et al.Identification of Polycystic Ovary Syndrome(PCOS)Specific Genes in Cumulus and Mural Granulosa Cells[J].PLo S One,2016,11(12):e0168875.
[2]姜晓琳,张兵,侯海燕,等.二甲双胍联合膈下逐瘀汤对多囊卵巢综合征大鼠炎性因子及性激素水平的影响[J].北京中医药大学学报,2018,41(1):65-70.
[3]Jiao J,Shi B,Wang T,et al.Characterization of long non-coding RNA and messenger RNA profiles in follicular fluid from mature and immature ovarian follicles of healthy women and women with polycystic ovary syndrome[J].Hum Reprod,2018,33(9):1735-1748.
[4]黄威,鲁耀邦,熊桦,等.补肾化瘀方对多囊卵巢综合征大鼠血清25羟基维生素D3、AMH、T、INS及E2的影响[J].湖南中医药大学学报,2018,38(6):650-652.
[5]Mao Z,Fan L,Yu Q,et al.Abnormality of Klotho Signaling Is Involved in Polycystic Ovary Syndrome[J].Reprod Sci,2018,25(3):372-383.
[6]和梦珂,张静,李昕,等.苍附导痰汤对米非司酮诱导PCOS大鼠卵巢形态及雄激素的影响[J].湖南中医药大学学报,2018,38(8):862-865.
[7]Mehdinejadiani S,Amidi F,Mehdizadeh M,et al.The effects of letrozole and clomiphene citrate on ligands expression of Wnt3,Wnt7a,and Wnt8b in proliferative endometrium of women with Polycystic ovarian syndrome[J].Gynecol Endocrinol,2018,34(9):775-780.
[8]Mondal K,Chakraborty P,Kabir S N.Hyperhomocysteinemia and hyperandrogenemia share PCSK9-LDLR pathway to disrupt lipid homeostasis in PCOS[J].Biochem Biophys Res Commun,2018,503(1):8-13.
[9]Mehdinejadiani S,Amidi F,Mehdizadeh M,et al.The effects of letrozole and clomiphene citrate on ligands expression of Wnt3,Wnt7a,and Wnt8b in proliferative endometrium of women with Polycystic ovarian syndrome[J].Gynecol Endocrinol,2018,34(9):775-780.
[10]Qiao GY,Dong BW,Zhu CJ,et al.Deregulation of WNT2/FZD3/beta-catenin pathway compromises the estrogen synthesis in cumulus cells from patients with polycystic ovary syndrome[J].Biochem Biophys Res Commun,2017,493(1):847-854.
[11]Mehdinejadiani S,Amidi F,Mehdizadeh M,et al.Effects of letrozole and clomiphene citrate on Wnt signaling pathway in endometrium of polycystic ovarian syndrome and healthy womendagger[J].Biol Reprod,2019,100(3):641-648.
[12]Wu XQ,Wang YQ,Xu SM,et al.The WNT/beta-catenin signaling pathway may be involved in granulosa cell apoptosis from patients with PCOS in North China[J].J Gynecol Obstet Hum Reprod,2017,46(1):93-99.
[13]何轶然,张治芬,王芳,等.SIRT1、Fox O3a在DHEA诱导多囊卵巢综合征模型大鼠卵巢组织中的表达及意义[J].浙江医学,2018,40(5):429-432,438,后插1.
[14]Jiao J,Shi B,Wang T,et al.Characterization of long non-coding RNA and messenger RNA profiles in follicular fluid from mature and immature ovarian follicles of healthy women and women with polycystic ovary syndrome[J].Hum Reprod,2018,33(9):1735-1748.
[15]Aydos A,Gurel A,Oztemur Islakoglu Y,et al.Identification of Polycystic Ovary Syndrome(PCOS)Specific Genes in Cumulus and Mural Granulosa Cells[J].PLo S One,2016,11(12):e0168875.