Increased Expression of 11<i>β</i>-Hydroxysteroid Dehydrogenase Type 1 in Experimental Periodontitis Induced by Lipopolysaccharide from <i>Porphyromonas gingivalis</i>

It has been proposed that 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), which activates glucocorticoids, plays a role in chronic inflammatory diseases including metabolic diseases, rheumatoid arthritis, and ulcerative colitis. We have recently reported that the expression of 11β-HSD1 is increased in the gingiva of patients with chronic periodontitis and in that of rats with ligature-induced periodontitis. In this study, to further demonstrate the involvement of 11β-HSD1 in chronic periodontitis, the expression of 11β-HSD1 was investigated in another rat model of experimental periodontitis induced by intragingival injection of lipopolysaccharide from Porphyromonas gingivalis (LPS-PG). Alveolar bone loss was observed two weeks after intragingival injection of LPS-PG. The level of 11β-HSD1 mRNA assessed by real-time reverse transcriptase-polymerase chain reaction was significantly elevated in LPS-PG-induced periodontitis compared with controls. The expression of 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), which inactivates glucocorticoids, was not significantly different between control and LPS-PG-induced periodontitis. The expression of 11β-HSD1 was significantly correlated with that of TNF in LPS-PG-induced periodontitis. The increased expression of 11β-HSD1 protein in LPS-PG-induced periodontitis was confirmed by immunohistochemistry using anti-11β-HSD1 antibody. These results further suggest a role for 11β-HSD1 in the pathogenesis of chronic periodontitis.

Therapeutic Potential of Thunbergia laurifolia L.Extract in Gestational Diabetes Mellitus:Insights from a Rat Model

Objective:To assess the effects of Thunbergia laurifolia L.extract(TLE)on gestational diabetes mellitus(GDM)in a rat model.Methods:Thunbergia laurifolin L.leaves were subjected to ethanolic extraction.In vivo study,50 pregnant rats were randomly divided into 5 groups(10 for each):non-GDM group,GDM induced by streptozotocin(STZ,60 mg/kg i.p.),metformin(MET)100 mg/kg,TLE 50,and 500 mg/kg groups.Administration was performed on gestation day 7 until term(day 21).The effects of TLE on blood glucose,insulin levels,lipid profiles,liver enzymes,and maternal performances were assessed.In in vitro study,the effect of TLE was examined using the organ bath for uterine force measurement.Results:In in vivo study,TLE significantly reduced blood glucose as compared to GDM(P<0.05)with gradually increased insulin level.This effect was consistent with islets of Langerhans restoration.Histologically,the uterine muscular layer displayed a marked increase in fiber area in response to both doses as compared to GDM(P<0.05).Additionally,TLE significantly reduced total cholesterol,triglyceride,and alanine transaminase levels(P<0.05).Intriguingly,TLE also led to a notable augmentation in gravid uterus size,live fetuses count,and implantation numbers,while significantly reducing the post-implantation loss rate associated with fetal classification(P<0.05).Thus,GDM improvements were close to those produced by MET.In in vitro study,TLE exerted a concentration-dependent inhibition of spontaneous uterine contractility(half-maximal inhibition concentration=1.2 mg/L).This inhibitory effect extended to potassium chloride depolarization and oxytocin-mediated contractions.When combined with its major constituent,rosmarinic acid,TLE produced an enhanced inhibitory effect(P<0.05).Conclusions:TLE ameliorated blood glucose levels,enhanced uterine muscular structure,and improved maternal and fetal performance in GDM.TLE also displayed tocolytic properties.These findings underscore the need for further exploration of TLE as a potential tocolytic agent to mitigate GDM-associated complications.