Effect Of Proanthocyanidin B2 On Experimental Diabetic Periodontitis In Rats

【Object】A diabetic periodontitis rat model was established to measure the periodontal probing depth（PD）and attachment loss（AL）,and to detect the expression of related inflammatory factors and apoptosis proteins in the gingival tissue of the rats,so as to explore the effect of GSPB2 on diabetic periodontitis and preliminarily explore its mechanism.【Methods】Selected 60 male SD rats were randomly divided into:healthy control group（group H,15）periodontitis group（P group,15）and diabetes periodontitis group（DP group,30）.Periodontal ligation+high glucose diet was used to establish the periodontitis rat model.Periodontal ligation+high glucose and high fat diet+intritoneal injection of streptozotocin（STZ,30mg/kg）was used to establish the diabetic periodontitis rat model.After 8 weeks of modeling,3 rats in each group were randomly selected to measure blood glucose,PD and AL of maxillary second molars,and the periodontal tissue morphology was observed by HE staining of the mandibular tissue blocks around the maxillary second molars.After modeling,the DP group randomly divided into two groups（DP1,DP2）,continuous lavage for eight weeks,DP2 given150mg/（kg·d）GSPB2 solution,DP1 group and H group were given equal normal saline.The PD and AL of maxillary second molars were measured.The expression of TNF-αand IL-1βin gingival tissue was detected by immunohistochemical staining.The expression of Bcl-2,Cytochrome C and Caspase-9 in the gingival tissues was detected by Western blot.Mitochondrial ultrastructure of gingival tissue cells was observed by electron microscopy,and apoptosis of gingival tissue cells was observed by TUNEL staining.【Results】The blood glucose level of DP group was significantly higher than that of H group,and the difference was statistically significant（P<0.05）.The average blood glucose of rats in DP group>16.5mmol/L,with signs of polydipsia,polyuria,etc.,indicating successful diabetes modeling.PD and AL in P and DP groups were significantly higher than those in H group,and the difference was statistically significant（P<0.05）,and the DP group was higher than P group,the difference was statistically significant（P<0.05）.Histological observation showed that:the P group and the DP group presented different degrees of periodontal damage,inflammatory cell infiltration in the gingival lamina propria,combined with the proliferation of epithelial root to form the periodontal pocket,the periodontal membrane fiber arrangement was disorderly,and the absorption of alveolar crest was damaged,and the DP group was more serious,suggesting that the periodontitis modeling was successful.After gavage,the expression of TNF-αand IL-1βin gingival tissue of group DP1 was higher than that of group DP2,and the difference was statistically significant（P<0.05）.Compared with group H₀,the expression of Bcl-2 in gingival tissues of rats in DP1 group was decreased,while the expression of cytochrome C and Caspase-9 was up-regulated,and the difference was statistically significant（P<0.05）,apoptosis rate of gingival tissue cells was significantly increased,and the difference was statistically significant（P<0.05）,mitochondrial ultrastructure was damaged.In DP2 group,the expression of cytochrome C and caspase-9 decreased,the expression of Bcl-2 increased,and the difference was statistically significant（P<0.05）,the apoptosis rate of gingival tissue cells was significantly lower than that of DP1 group,and the difference was statistically significant（P<0.05）,and the normal ultrastructure of mitochondria was restored.【Conclusion】The periodontitis model was successfully established by ligation combined with diet.On this basis,the periodontitis model of type 2 diabetes combined with STZ injection could be successfully established.Periodontitis alone does not cause an increase in blood glucose,but diabetic status will aggravate periodontal inflammation.GSPB2 can improve the periodontitis and alveolar bone destruction in diabetic periodontitis rats.GSPE2 has a protective effect on diabetic periodontitis,and the mechanism may be related to the inhibition of cell apoptosis in gingival tissue.