AIMS Inflammation was closely associated with diabetes-related endothelial dysfunction. C1q/tumor necrosis factor-related protein 3 (CTRP3) is a member of the CTRP family and can provide cardioprotection in many cardiovascular diseases via suppressing the production of inflammatory factors. However, the role of CTRP3 in high glucose- (HG-) related endothelial dysfunction remains unclear. This study evaluates the effects of CTRP3 on HG-induced cell inflammation and apoptosis. MATERIALS AND METHODS To prevent high glucose-induced cell injury, human umbilical vein endothelial cells (HUVECs) were pretreated with recombinant CTRP3 for 1 hour followed by normal glucose (5.5 mmol/l) or high glucose (33 mmol/l) treatment. After that, cell apoptosis and inflammatory factors were determined. RESULTS Our results demonstrated that CTRP3 mRNA and protein expression were significantly decreased after HG exposure in HUVECs. Recombinant human CTRP3 inhibited HG-induced accumulation of inflammatory factors and cell loss in HUVECs. CTRP3 treatment also increased the phosphorylation levels of protein kinase B (AKT/PKB) and the mammalian target of rapamycin (mTOR) in HUVECs. CTRP3 lost its inhibitory effects on HG-induced cell inflammation and apoptosis after AKT inhibition. Knockdown of endogenous CTRP3 in HUVECs resulted in increased inflammation and decreased cell viability in vitro. CONCLUSIONS Taken together, these findings indicated that CTRP3 treatment blocked the accumulation of inflammatory factors and cell loss in HUVECs after HG exposure through the activation of AKT-mTOR signaling pathway. Thus, CTRP3 may be a potential therapeutic drug for the prevention of diabetes-related endothelial dysfunction.

中文翻译：

---

CTRP3 保护人脐静脉内皮细胞免受高糖诱导的细胞损伤。

AIMS 炎症与糖尿病相关的内皮功能障碍密切相关。C1q/肿瘤坏死因子相关蛋白 3 (CTRP3) 是 CTRP 家族的成员，可通过抑制炎症因子的产生在许多心血管疾病中提供心脏保护。然而，CTRP3 在高糖 (HG-) 相关的内皮功能障碍中的作用仍不清楚。本研究评估了 CTRP3 对 HG 诱导的细胞炎症和细胞凋亡的影响。材料与方法为防止高糖诱导的细胞损伤，用重组CTRP3预处理人脐静脉内皮细胞（HUVECs）1小时，然后进行正常葡萄糖（5.5 mmol/l）或高糖（33 mmol/l）处理。之后，测定细胞凋亡和炎症因子。结果 我们的结果表明，HUVECs 中 HG 暴露后 CTRP3 mRNA 和蛋白质表达显着降低。重组人 CTRP3 抑制 HG 诱导的 HUVECs 中炎症因子的积累和细胞损失。CTRP3 处理还增加了 HUVEC 中蛋白激酶 B (AKT/PKB) 和雷帕霉素哺乳动物靶标 (mTOR) 的磷酸化水平。CTRP3在AKT抑制后失去了对HG诱导的细胞炎症和细胞凋亡的抑制作用。HUVEC 中内源性 CTRP3 的敲除导致体外炎症增加和细胞活力降低。结论 综上所述，这些发现表明 CTRP3 治疗通过激活 AKT-mTOR 信号通路阻断了 HG 暴露后 HUVEC 中炎症因子的积累和细胞损失。因此，