Caffeic acid phenethyl ester (CAPE) is used as a therapeutic agent to prevent bone loss. We determined the effects of systemically administered CAPE on alveolar bone loss and oxidative stress in diabetic rats with experimental periodontitis. Forty male rats were divided into four equal groups: control, experimental periodontitis (EP), EP-diabetes mellitus (EP-DM) and EP-DM-CAPE. DM was induced by streptozotocin, then lipopolysaccharide was injected to induce periodontitis. CAPE was administered to the EP-DM-CAPE group daily for 15 days. Then, serum samples were taken and the rats were sacrificed for histological analyses. Serum interleukin (IL-1β) and oxidative stress also were evaluated. Alveolar bone loss was assessed histomorphometrically. Alveolar bone loss and IL-1β levels were significantly less in the EP-DM-CAPE and EP groups compared to the EP-DM group. Oxidative stress was significantly less in the EP-DM-CAPE group compared to the EP and EP-DM groups. Receptor activator of nuclear factor kappa-B ligand (RANKL) levels were significantly higher in the EP-DM group compared to the disease groups. CAPE significantly reduced RANKL levels in the EP-DM-CAPE group compared to the EP-DM group. We found that CAPE treatment significantly inhibited DM induced oxidative stress and RANKL induced osteoclastogenesis and alveolar bone loss in diabetic rats with periodontitis.

咖啡酸苯乙酯（CAPE）用作预防骨丢失的治疗剂。我们确定了全身给药的CAPE对患有实验性牙周炎的糖尿病大鼠的牙槽骨损失和氧化应激的影响。将40只雄性大鼠分为四个相等的组：对照组，实验性牙周炎（EP），EP-糖尿病（EP-DM）和EP-DM-CAPE。链脲佐菌素诱导DM，然后注射脂多糖诱导牙周炎。将CAPE每天给予EP-DM-CAPE组15天。然后，采集血清样品并处死大鼠以进行组织学分析。还评估了血清白介素（IL-1β）和氧化应激。肺泡骨丢失通过组织形态学评估。与EP-DM组相比，EP-DM-CAPE和EP组的牙槽骨丢失和IL-1β水平明显降低。与EP和EP-DM组相比，EP-DM-CAPE组的氧化应激显着降低。与疾病组相比，EP-DM组的核因子κB配体（RANKL）受体激活剂水平明显更高。与EP-DM组相比，CAPE可以显着降低EP-DM-CAPE组的RANKL水平。我们发现，CAPE治疗可显着抑制糖尿病性牙周炎大鼠的DM诱导的氧化应激和RANKL诱导的破骨细胞生成和牙槽骨丢失。与疾病组相比，EP-DM组的核因子κB配体（RANKL）受体激活剂水平明显更高。与EP-DM组相比，CAPE显着降低了EP-DM-CAPE组的RANKL水平。我们发现，CAPE治疗可显着抑制糖尿病性牙周炎大鼠的DM诱导的氧化应激和RANKL诱导的破骨细胞生成和牙槽骨丢失。与疾病组相比，EP-DM组的核因子κB配体（RANKL）受体激活剂水平明显更高。与EP-DM组相比，CAPE可以显着降低EP-DM-CAPE组的RANKL水平。我们发现，CAPE治疗可显着抑制糖尿病性牙周炎大鼠的DM诱导的氧化应激和RANKL诱导的破骨细胞生成和牙槽骨丢失。