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This study aimed to investigate the functional restoration of radiation-damaged salivary gland with human amniotic epithelial cells (hAECs) transplantation by intra-glandular injection. hAECs were isolated from the amnion tissues. After primary culture, the phenotype of hAECs of the second passage was identified by flow cytometry (FCM) and immunocytochemical staining. Then, hAECs were intra-glandularly injected into the irradiated glands of mice. At different time points after transplantation, the glands were collected for hematoxylin-eosin (HE) staining and immunofluorescence staining, and the saliva flow rate was also determined. Results showed these cells were positive for CD29, CD73 and CK19 and negative for CD44, CD34, CD45 and CD71. The transplanted hAECs in the recipient glands could differentiate into acinar-like cells and resulted in morphological and functional restoration of salivary gland.

Objective: To explore the protective effect of human urine‐derived stem cell exosomes (hUSC‐Exos) on radiation‐induced salivary gland (SG) injuries in Sprague Dawley rats. Methods: Fresh adult urine was collected, and primary hUSCs were isolated and identified. The hUSCs were hypoxia‐pretreated with 1% oxygen for 24 h and then transferred to a normoxic culture environment for 24 h. The hUSC‐Exos were collected and identified for exosomes. A radiation‐induced injury model was established in the rats, and exosomes were introduced by local injection in the SG and tail vein. The submandibular gland was excised for morphological observation 1 week later. Immunohistochemical detection of the glandular tissue was conducted by α‐smooth muscle actin (a‐SMA), stem cell growth factor receptor (c‐Kit) staining, and periodic acid–Schiff staining. Qualitative polymerase chain reaction and western blot analysis were adopted to detect the gene and protein expression of Wnt3a, GSK3β, and Axin. Results: In both the normoxic and hypoxic hUSC‐Exo groups, microvesicular structures with bilayer membranes of approximately 80 nm in diameter were detected, and the expressions of CD9 and CD63 were detected by nanoflow cytometry. Compared with the control group, in the radiation‐induced injury model group, the expression of a‐SMA was significantly higher, the expression of c‐Kit was significantly lower, and the expressions of Wnt3a, GSK3β, and Axin were significantly upregulated; the differences were statistically significant (p < 0.05). Compared with the model group, in the normoxic and hypoxic hUSC‐Exo groups, the expression of a‐SMA was significantly decreased, the expression of c‐Kit was significantly increased, and the expressions of Wnt3a, GSK3β, and Axin were significantly upregulated; the differences were statistically significant (p < 0.05). Conclusion: Hypoxia‐pretreated hUSC‐Exos could repair radiation‐induced SG injuries by activating the Wnt3a/GSK3β pathway to suppress the expressions of a‐SMA and c‐Kit. [ABSTRACT FROM AUTHOR]