中华妇产科杂志
中華婦產科雜誌
중화부산과잡지
CHINESE JOUNAL OF OBSTETRICS AND GYNECOLOGY
2011年
6期
441-445
,共5页
内毒素类%青春期%生殖,月经周期,卵巢%交感神经系统,大鼠
內毒素類%青春期%生殖,月經週期,卵巢%交感神經繫統,大鼠
내독소류%청춘기%생식,월경주기,란소%교감신경계통,대서
Endotoxins%Puberty%Reproduction%Menstrual cycle%Ovary%Sympathetic nervous system%Rats
目的 研究生命早期的免疫应激对雌鼠青春期生殖功能的影响.方法 雌性Sprague-Dawley大鼠在出生后第3、5天行腹腔注射脂多糖(50 μg/kg)和生理盐水作为实验组和对照组.每周测体质量,生后30 d开始监测青春期启动(即阴道口初开放)时间和卵巢周期的变化.生后6周行卵巢切除术,观察卵巢组织形态学的变化(卵泡内膜厚度和各种类型卵泡的数目);用免疫组化方法测定卵巢交感神经兴奋性的改变[以低亲和力的神经生长因子受体(p75NGFR)的免疫染色强度表示].结果 生命早期的免疫应激(暴露于脂多糖),能延迟阴道口初开放的时间,实验组大鼠为生后(40.6±0.7)d,对照组为生后(38.6±0.6)d,两组比较,差异有统计学意义(P＜0.05);降低卵巢正常周期的比例,实验组为26.1%,对照组为66.8%,两组比较,差异有统计学意义(P＜0.05);减少各种类型卵泡的数目,实验组大鼠原始卵泡(610±47)个、初级卵泡(624±41)个、窦前卵泡(183±16)个、窦卵泡(32±4)个,对照组分别为(1181±57)、(960±30)、(260±14)、(79±7)个,分别比较,差异均有统计学意义(P＜0.05);增加卵泡内膜厚度,实验组及对照组分别为(15.8±0.4)、(11.4±0.3)μm,两组比较,差异有统计学意义(P＜0.05).实验组大鼠的卵巢p75NGFR免疫染色强度较对照组明显增高(P＜0.05).结论 雌鼠生命早期的免疫应激对其青春期的生殖功能有明显的影响.生命早期的免疫应激可能通过上调卵巢交感神经兴奋性而推迟青春期发育,并减少卵巢正常周期的比例和卵泡储备,使卵泡内膜增厚.
目的 研究生命早期的免疫應激對雌鼠青春期生殖功能的影響.方法 雌性Sprague-Dawley大鼠在齣生後第3、5天行腹腔註射脂多糖(50 μg/kg)和生理鹽水作為實驗組和對照組.每週測體質量,生後30 d開始鑑測青春期啟動(即陰道口初開放)時間和卵巢週期的變化.生後6週行卵巢切除術,觀察卵巢組織形態學的變化(卵泡內膜厚度和各種類型卵泡的數目);用免疫組化方法測定卵巢交感神經興奮性的改變[以低親和力的神經生長因子受體(p75NGFR)的免疫染色彊度錶示].結果 生命早期的免疫應激(暴露于脂多糖),能延遲陰道口初開放的時間,實驗組大鼠為生後(40.6±0.7)d,對照組為生後(38.6±0.6)d,兩組比較,差異有統計學意義(P＜0.05);降低卵巢正常週期的比例,實驗組為26.1%,對照組為66.8%,兩組比較,差異有統計學意義(P＜0.05);減少各種類型卵泡的數目,實驗組大鼠原始卵泡(610±47)箇、初級卵泡(624±41)箇、竇前卵泡(183±16)箇、竇卵泡(32±4)箇,對照組分彆為(1181±57)、(960±30)、(260±14)、(79±7)箇,分彆比較,差異均有統計學意義(P＜0.05);增加卵泡內膜厚度,實驗組及對照組分彆為(15.8±0.4)、(11.4±0.3)μm,兩組比較,差異有統計學意義(P＜0.05).實驗組大鼠的卵巢p75NGFR免疫染色彊度較對照組明顯增高(P＜0.05).結論 雌鼠生命早期的免疫應激對其青春期的生殖功能有明顯的影響.生命早期的免疫應激可能通過上調卵巢交感神經興奮性而推遲青春期髮育,併減少卵巢正常週期的比例和卵泡儲備,使卵泡內膜增厚.
목적 연구생명조기적면역응격대자서청춘기생식공능적영향.방법 자성Sprague-Dawley대서재출생후제3、5천행복강주사지다당(50 μg/kg)화생리염수작위실험조화대조조.매주측체질량,생후30 d개시감측청춘기계동(즉음도구초개방)시간화란소주기적변화.생후6주행란소절제술,관찰란소조직형태학적변화(란포내막후도화각충류형란포적수목);용면역조화방법측정란소교감신경흥강성적개변[이저친화력적신경생장인자수체(p75NGFR)적면역염색강도표시].결과 생명조기적면역응격(폭로우지다당),능연지음도구초개방적시간,실험조대서위생후(40.6±0.7)d,대조조위생후(38.6±0.6)d,량조비교,차이유통계학의의(P＜0.05);강저란소정상주기적비례,실험조위26.1%,대조조위66.8%,량조비교,차이유통계학의의(P＜0.05);감소각충류형란포적수목,실험조대서원시란포(610±47)개、초급란포(624±41)개、두전란포(183±16)개、두란포(32±4)개,대조조분별위(1181±57)、(960±30)、(260±14)、(79±7)개,분별비교,차이균유통계학의의(P＜0.05);증가란포내막후도,실험조급대조조분별위(15.8±0.4)、(11.4±0.3)μm,량조비교,차이유통계학의의(P＜0.05).실험조대서적란소p75NGFR면역염색강도교대조조명현증고(P＜0.05).결론 자서생명조기적면역응격대기청춘기적생식공능유명현적영향.생명조기적면역응격가능통과상조란소교감신경흥강성이추지청춘기발육,병감소란소정상주기적비례화란포저비,사란포내막증후.
Objective To investigate the long-term programming effects on pubertal reproductive function by immunological challenge in early life. Methods Female Sprague-Dawley rats were administered by endotoxin (lipopolysaccharide, LPS) at a dosage of 50 μg/kg and saline intraperitoneally on postnatal day 3 and 5. Body weight was measured weekly. Puberty onset ( vaginal opening) and oestrous cyclicity were monitored from postnatal day 30. At the age of 6 weeks, bilateral ovariectomy was performed. The histological and morphological change of the ovaries (the thickness of the theca interna and the number of different kinds of follicles) were observed and the immunoreactivity of the ovarian sympathetic nerve markers (low affinity receptor of nerve growth factor, p75NGFR) was evaluated by immune staining. Results Immunological challenge (exposed to LPS) in early life delayed vaginal opening significantly [LPS-treated (40.6 ±0.7) days versus controls ( 38. 6 ± 0. 5 ) days, P ＜ 0. 05], decreased the percentage of normal oestrous cyclicity ( LPS-treated 26. 1% versus controls 66. 8% , P＜ 0. 05 ) , decreased the total number of different types of follicles (primordial follicles: LPS-treated 610 ±47 versus controls 1181 ±57, P ＜ 0. 05; primary follicles: LPS-treated 624 ±41 versus controls 960 ± 30, P ＜ 0. 05 ; preantral follicles: LPS-treated 183 ± 16 versus controls 260 ± 14, P ＜ 0. 05; antral follicles: LPS-treated 32 ± 4 versus controls 79 ± 7, P ＜ 0. 05) and increased the thickness of the theca interna [LPS-treated ( 15. 8 ±0. 4) μm versus controls (11.4 ±0. 3) μm, P ＜ 0. 05]. The immunostaining of p75NGFR was obviously enhanced in the LPS-treated ovaries when compared with that of controls ( P ＜ 0. 05 ) . Conclusions Immunological stress during early critical developmental windows could have long dysfunctional effects on the pubertal reproductive function. It delayed puberty onset, reduced the percentage of the normal oestrous cycles, decreased follicles reserve and increased the thickness of the theca interna which might involve the up-regulation of the local ovarian sympathetic nerve activity.
