International dental journal · 2026
Dicliptera Chinensis Polysaccharide Alleviates Radiation-Induced Submandibular Gland Injury Through Microvessel Protection and the Regulation of Apoptosis.
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Zhao Yanfei, Liu Zhiqing, Huang Yude, Zhao Lixiang, Gao Linjing, Wang Xian, Wang Yuetong, Li Yuetao, Nong Xiaolin, Wang Daiyou
Аннотация
OBJECTIVE: To investigate the protective effect and mechanism of Dicliptera chinensis polysaccharide (DCP) on radiation-induced submandibular gland injury via regulating microvascular injury and apoptosis.
MATERIALS AND METHODS: A rat model of radiation-induced submandibular gland injury was established by delivering a single 18 Gy dose via linear accelerator irradiation. Model validation and the intervention effects of DCP were evaluated by assessing salivary flow rate, submandibular gland index, and histopathological changes. Immunohistochemistry was performed to detect the expression of vascular functional markers VEGF and CD31 in submandibular gland tissues. In vitro, human umbilical vein endothelial cells (HUVECs) were exposed to 10 Gy X-ray irradiation to establish an endothelial radiation injury model. Western blot was used to detect the expression of PI3K/AKT pathway-related proteins in HUVECs, and immunofluorescence staining was applied to quantitatively determine the expression level of phosphorylated AKT (p-AKT). The regulatory effects of DCP on endothelial apoptosis-related proteins and vascular-related proteins were further verified at the cellular level.
RESULTS: DCP intervention preserved salivary gland secretory function, attenuated histopathological damage and fibrosis, and suppressed cell apoptosis. These effects were accompanied by significantly upregulated CD31 and VEGF expression, increased microvessel density, and amelioration of radiation-induced microvascular impairment.
CONCLUSION: DCP alleviated radiation-induced submandibular gland injury, inhibited cell apoptosis, and improved microvascular dysfunction. This radioprotective effect may be mediated through regulation of the PI3K/AKT signaling pathway and the upregulation of VEGF and CD31.
MATERIALS AND METHODS: A rat model of radiation-induced submandibular gland injury was established by delivering a single 18 Gy dose via linear accelerator irradiation. Model validation and the intervention effects of DCP were evaluated by assessing salivary flow rate, submandibular gland index, and histopathological changes. Immunohistochemistry was performed to detect the expression of vascular functional markers VEGF and CD31 in submandibular gland tissues. In vitro, human umbilical vein endothelial cells (HUVECs) were exposed to 10 Gy X-ray irradiation to establish an endothelial radiation injury model. Western blot was used to detect the expression of PI3K/AKT pathway-related proteins in HUVECs, and immunofluorescence staining was applied to quantitatively determine the expression level of phosphorylated AKT (p-AKT). The regulatory effects of DCP on endothelial apoptosis-related proteins and vascular-related proteins were further verified at the cellular level.
RESULTS: DCP intervention preserved salivary gland secretory function, attenuated histopathological damage and fibrosis, and suppressed cell apoptosis. These effects were accompanied by significantly upregulated CD31 and VEGF expression, increased microvessel density, and amelioration of radiation-induced microvascular impairment.
CONCLUSION: DCP alleviated radiation-induced submandibular gland injury, inhibited cell apoptosis, and improved microvascular dysfunction. This radioprotective effect may be mediated through regulation of the PI3K/AKT signaling pathway and the upregulation of VEGF and CD31.