Effects of oral fibroblast growth factor FGF-1 on PCNA protein and submandibular gland degeneration in diabetic patients

ZHONG Cui-cui; ZHANG Yi-xi; CHEN Gui-ying

doi:10.3969/j.issn.1672-2973.2018.01.004

Abstract：Objective:To study effects of oral fibroblast growth factor FGF-1 on PCNA protein and submandibular gland degeneration in diabetic patients.Method:Twenty male db/db mice were randomly divided into two groups:experimental group and model group,and 10 8-week-old male db/m mice were selected as control group.The weight of the mice was measured at 0 weeks,4 weeks,8 weeks,12 weeks and 16 weeks respectively.The blood glucose meter was used to measure blood glucose in mice.Saliva flow rate was used to measure saliva flow in mice.Using the HE staining method to observe the distribution of submandibular gland vesicular cells and the functional cavity.Immunohistochemistry was used to observe the distribution of submandibular gland vesicles and catheters.Result:The blood glucose and weight of mice in the experimental group decreased significantly in the test of 0-4 weeks (P＜0.05).and gradually stabilized in the later stage.But the model group had no significant change (P＞0.05).The saliva flow rate of the experimental group showed an increasing trend,with the highest flow rate reaching 308± 34.0mg · min-1 · kg-1.It was significantly higher than that of the control group (P＜0.05).HE staining results show clear submandibular tissue structure in the experimental group.Severe adenovesicles and catheter atrophy were seen in the model group.Immunohistochemical results showed that the positive rate of PCNA cells in the experimental group was significantly higher than that in the model group (P＜0.05),but still significantly lower than the blank control group (P＜0.05).Conclusions:PGF-1 factor can significantly increase the positive rate of PCNA cells in submandibular gland of mice,balance the blood sugar and body weight of diabetic mice,and have a positive significance in reversing the degeneration of submandibular gland function.