动物造模 z-bio 2021-09-07 235

　　Objective: To study the damage effect and possible molecular mechanism of PM2.5 (particulate matter with aerodynamic diameter ≤2.5μm) on rat uterus in short-term exposure.

　　Methods: Thirty female SD rats were randomly divided into a normal saline control group, a 1.5 mg/(kg·bw) PM2.5 low-dose exposure group, and a 6mg/(kg·bw) PM2.5 high-dose exposure group, and they were continuously exposed for 30 days. . The pathological examination of HE staining observed the damage of uterine tissue after PM2.5 exposure. The TUNEL method and the method of detecting the expression of cleaved caspase-3 protein were used to observe the apoptosis of rat uterine tissues in each group. Fluorescence quantitative PCR was used to detect the mRNA expression levels of glucose regulatory protein 78 (GRP78), protein kinase-like endoplasmic reticulum kinase (PERK), eukaryotic translation initiation factor 2α (eIF2α) and C/EBP homologous protein (CHOP) in the uterus. Western blot was used to detect the expression levels of stress-related proteins in the endoplasmic reticulum of the uterus.

　　Results: After a short-term exposure to PM2.5, endometrial epithelial cells atrophy, the intercellular space increases, and the cells appear vacuolization; at the same time the glands also appear atrophy. TUNEL test results showed that the apoptosis rate of uterine tissue cells in the control group was (9.93±1.66)%, and the apoptosis rate of uterine tissue cells in the low-dose and high-dose exposure groups were (29.40±6.96)% and (43.58±8.23), respectively. )%, the apoptosis rate of the exposed group was significantly higher than that of the control group, and the difference was statistically significant (P<0.05). Compared with the control group, the GRP78, PERK, eIF2α and CHOP gene and protein expression levels in the uterus of the exposed group were significantly increased, and the difference was statistically significant (P<0.05). The expression of cleaved caspase-3 protein in the uterus of the exposed group was significantly higher than that of the control group (P<0.05).

　　Conclusion: Short-term exposure to PM2.5 can damage the morphology of rat uterine tissue. The mechanism of action may be related to the PERK-eIF2α-CHOP signaling pathway that mediates the endoplasmic reticulum stress response in uterine tissue and induces cell apoptosis in uterine tissue.