Abstract
Background: Most patients with thyroid cancer suffer from salivary gland (SG) dysfunctions after radioiodine (RI) therapy. We investigated the effects of keratinocyte growth factor (KGF)-1 on RI-induced SG dysfunction in an animal model. Methods: Six C57BL/6 mice were assigned to each of the following groups: treatment naïve control group, RI group, and RI+KGF-1 group. Body and SG weights, salivary flow rates, salivary lag times and changes in 99mTc pertechnetate uptake and excretion were measured, and histologic changes were noted. Amylase activities and epidermal growth factor (EGF) concentrations in saliva were also measured. In addition, TUNEL assays were performed and apoptosis-related protein expressions were assessed. Results: RI-induced reductions in salivary flow rates and increases in salivary lag times observed in the RI group were not observed in RI+KGF-1 group. Mice in RI group had higher HIF1a levels than controls, but HIF1a levels in RI+KGF-1 group were similar to those in control group. Furthermore, mice in RI+KGF-1 group had more mucin stained acini and decreased periductal fibrosis than mice in RI group, and tissue remodeling of many salivary epithelial cells (AQP5) and endothelial cells (CD31) were observed in RI+KGF-1 group. Amylase activity and expression in saliva were greater in RI+KGF-1 group than in RI group, and fewer apoptotic cells were observed in RI+KGF-1 group. Furthermore, BCLxl (anti-apoptotic) expression was higher, and Bax (pro-apoptotic) expression was lower in RI+KGF-1 group than in RI group. Conclusions: Local delivery of KGF-1 might prevent RI-induced SG damage by reducing apoptosis.
Highlights
Salivary gland (SG) dysfunction is commonly encountered after radioiodine (RI) treatment for differentiated thyroid cancer and causes xerostomia, swallowing difficulties, oral candidiasis, taste loss, and tooth decay
We investigated the effect of keratinocyte growth factor (KGF)-1 on protecting RI-induced salivary gland (SG) dysfunction and sought to elucidate the mechanisms responsible for its radioprotective effect in a mouse model
Results presented as means than the RI+KGF-1 group
Summary
Salivary gland (SG) dysfunction is commonly encountered after radioiodine (RI) treatment for differentiated thyroid cancer and causes xerostomia, swallowing difficulties, oral candidiasis, taste loss, and tooth decay. Many studies have been undertaken to develop means of preventing RI-induced SG dysfunctions, and several treatments based on antioxidants, [1,2] stem cells [3], and bioactive factors [4,5] have been described in the literature. We investigated the effects of keratinocyte growth factor (KGF)-1 on RI-induced SG dysfunction in an animal model. Methods: Six C57BL/6 mice were assigned to each of the following groups: treatment naïve control group, RI group, and RI+KGF-1 group. Results: RI-induced reductions in salivary flow rates and increases in salivary lag times observed in the RI group were not observed in RI+KGF-1 group. Mice in RI group had higher HIF1a levels than controls, but HIF1a levels in
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