动物造模 z-bio 2022-06-24 415

　　OBJECTIVE: To study the damage effect and possible molecular mechanism of PM2.

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

　　Results: After short-term exposure to PM2.5, the endometrial epithelial cells atrophied, the intercellular space increased, and the cells appeared vacuolated; meanwhile, the glands also atrophied. The results of TUNEL test showed that the apoptosis rate of uterine tissue cells in the control group was (9.93±1.66)%, and the apoptosis rates 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, the difference was statistically significant (P<0.05). Compared with the control group, the gene and protein expression levels of GRP78, PERK, eIF2α and CHOP in the uterus of the exposure group were significantly increased, and the difference was statistically significant (P<0.05). The expression of cleaved caspase-3 protein in uterus of exposed group was significantly higher than that of control group (P<0.05).

　　Conclusion: Short-term exposure to PM2.5 can damage the morphology of uterine tissue in rats, and its mechanism may be related to the PERK-eIF2α-CHOP signaling pathway mediating endoplasmic reticulum stress response in uterine tissue, thereby inducing apoptosis in uterine tissue.