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目的探讨新生期脂多糖暴露对睾丸发育及波形蛋白表达和分布的影响。方法选取新生雄性SD大鼠150只,随机分为对照组和实验组,实验组于生后第4～12d期间,隔日皮下注射脂多糖(75μg/kg),共5次,对照组在相同时间皮下注射等容生理盐水。常规饲养至生后14d、21d、28d、包皮分离日、60d、77d分批取材,采用组织学和免疫组化技术,观察脂多糖对大鼠睾丸发育、波形蛋白的表达与分布的影响。结果①与同龄对照组相比,实验组大鼠生精小管横径变小,生精上皮变薄,细胞排列紊乱,生精细胞与支持细胞分离,脱落至管腔,性成熟以后,管腔内精子生成减少;②对照组波形蛋白阳性染色从基膜围绕支持细胞核形成棕黄色的环,并呈辐射状延伸至管腔;实验组支持细胞变矮、变圆,波形蛋白仅见于核周或核的基部胞质,伸向管腔的辐射状条带变短或消失。结论新生期脂多糖暴露,可改变支持细胞波形蛋白的有序分布,造成生精细胞脱落,干扰生精细胞的发育成熟,这种影响可延续至成年期,导致成年期精子生成减少。
Objective To investigate the effect of neonatal lipopolysaccharide exposure on testicular development and the expression and distribution of vimentin. Methods 150 newborn male Sprague-Dawley rats were randomly divided into control group and experimental group. The experimental group was injected subcutaneously with lipopolysaccharide (75μg / kg) every other day for 4 to 12 days, Subcutaneous injection of normal saline. Routine feeding to 14d, 21d, 28d after birth, foreskin on the day of separation, 60d, 77d batch draw, using histological and immunohistochemical techniques to observe the effects of lipopolysaccharide on rat testis development, the expression and distribution of vimentin. Results ① Compared with the same age control group, the diameter of seminiferous tubules in experimental group became smaller, the seminiferous epithelium became thinner and the cells arranged in disorder, the spermatocytes were separated from the supporting cells and dropped into the lumen. After sexual maturation, The formation of spermatozoa decreased; ② The control group vimentin positive staining from the basement membrane around the nucleus to form a brown-yellow ring, and radially extended to the lumen; experimental group supporting cells shorter, round, vimentin found only in the perinuclear or The basal cytoplasm of the nucleus, the radial bands extending toward the lumen, become shorter or disappear. Conclusions Exposure of neonatal lipopolysaccharide can change the orderly distribution of vimentin supporting cells, resulting in the shedding of spermatogenic cells and interfering with the development of spermatogenic cells. This effect may extend to adulthood, resulting in the reduction of spermatogenesis during adulthood.