动物造模 z-bio 2022-10-18 307

　　Objective To study the effect of ubiquitin carboxyl terminal hydrolase L1 gene deletion on the reproductive system of female mice.

　　Methods Vaginal smear, immunohistochemistry, Western blot and RNA interference were used to analyze the effects of UCH-L1 gene deletion on ovarian function and follicular development in mice.

　　Results The body weight of the homozygous adult female mice with UCH-L1 gene deletion was decreased, the movement was difficult, and the uterus was thin. The expression of UCH-L1 protein was not detected in the ovary and uterus of homozygous mice with UCH-L1 gene deletion. The ovarian volume was significantly smaller than that of heterozygous mice. There were some primitive follicles or atresia follicles in the ovarian cortex, and no mature follicles and corpus luteum. Reproductive key receptors such as estrogen receptor (ER), follicle stimulating hormone receptor (LHR), luteinizing hormone receptor (LHR) and progesterone receptor (PR) are expressed in the ovaries of homozygous and heterozygous UCHLl │ mice. The expression level of ER in the ovaries of homozygous mice is significantly lower than that of heterozygous mice. Down regulating the expression of UCH-LI in germinal vesicle (GV) oocytes by RNA interference can significantly reduce the maturation rate of oocytes.

　　Conclusion Female mice with UCH-L1 gene deletion do not have the ability to form mature follicles and ovulate, and the expression of ER in the ovary is significantly reduced. It is speculated that UCH-L1 may affect oocyte maturation and ovulation process by down regulating the expression of ER in ovary.