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Curcumin inhibits lipopolysaccharide and lipoteichoic acid-induced expression of proinflammatory cytokines and production of PGE 2 in the primary bubaline endometrial stromal cells
Molecular Biology Reports ( IF 2.8 ) Pub Date : 2020-11-10 , DOI: 10.1007/s11033-020-05961-y
Ajaz Ali 1 , Rouf Rashid Dar 1 , Sheikh Firdous Ahmad 2, 3 , Sanjay Kumar Singh 1 , Manas Kumar Patra 4 , Manjit Panigrahi 2 , Harendra Kumar 1 , Narayanan Krishnaswamy 5
Affiliation  

Infection of the uterus with Gram-positive Trueperella pyogenes and Gram-negative Escherichia coli is a common cause of postpartum endometritis in the cattle and buffalo and the condition is treated with antimicrobial drugs. The presence of drug residues in the milk and development of resistant bacteria necessitate the evaluation of alternate therapies for endometritis. Accordingly, we tested the immunomodulatory effect of curcumin in the bubaline endometrial stromal cells after treatment with the lipoteichoic acid (LTA) of Gram-positive Staphylococcus aureus and lipopolysaccharide (LPS) of Gram-negative E. coli that activate toll-like receptors (TLR-2 and TLR-4, respectively). Confluent primary culture of endometrial stromal cells was treated with LTA (1 µg/mL) and/or LPS (0.1 µg/mL), in the presence or absence of curcumin (30 µM for 24 h). PGE2 was assayed in the supernatant and the relative expression of proinflammatory cytokines (PICs) (IL1B, IL6, IL8 and TNFA) transcripts were quantified using real-time PCR. LTA was not effective in stimulating PGE2 production or upregulating the PIC expression except IL8. LTA+LPS increased PGE2 production and upregulated IL6 and IL8 genes. Curcumin inhibited the basal and LTA+LPS induced production of PGE2 and upregulation of PIC production. It was apparent that LPS, but not LTA, is a potent stimulator of PGE2 from the bubaline endometrial stromal cells. Curcumin downregulated the expression of LPS and/or LTA induced PICs and PGE2 and may be an alternate to antimicrobial drugs for the therapeutic management of endometritis.



中文翻译:

姜黄素抑制脂多糖和脂磷壁酸诱导的原发性子宫内膜基质细胞中促炎细胞因子的表达和PGE 2的产生

革兰氏阳性化脓性脓疱病和革兰氏阴性大肠杆菌感染子宫是牛和水牛产后子宫内膜炎的常见原因,该病可以用抗菌药物治疗。牛奶中药物残留的存在和耐药菌的产生,需要评估子宫内膜炎的替代疗法。因此,我们在用革兰氏阳性金黄色葡萄球菌的脂蛋白酸(LTA)和革兰氏阴性大肠杆菌的脂多糖(LPS)处理后,测试姜黄素在大肠子宫内膜基质细胞中的免疫调节作用激活toll样受体(分别为TLR-2和TLR-4)。在有或没有姜黄素(30 µM,24小时)的情况下,用LTA(1 µg / mL)和/或LPS(0.1 µg / mL)处理子宫内膜基质细胞的融合原代培养物。在上清液中检测PGE 2并使用实时PCR定量测定促炎细胞因子(PIC)(IL1B,IL6,IL8TNFA)转录本的相对表达。除IL8外,LTA不能有效刺激PGE 2的产生或上调PIC的表达。LTA + LPS增加PGE 2产生并上调IL6IL8基因。姜黄素抑制基础和LTA + LPS诱导的PGE 2的产生和PIC产生的上调。显然,LPS而不是LTA是来自子宫内膜间质基质细胞的PGE 2的有效刺激剂。姜黄素下调LPS和/或LTA诱导的PIC和PGE 2的表达,可能是治疗子宫内膜炎的抗菌药物的替代品。

更新日期:2020-11-12
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