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海带多糖对脂多糖致血管内皮细胞炎性反应的影响 被引量:4

The Effect of Laminaria Polysaecharide On Inflammatory Stress Induced By Lipopolysaccharide In Vascular Endothelial Cells
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摘要 目的:探讨海带多糖(LP)对脂多糖(LPS)致血管内皮细胞(Vascular endothelial cells,VECs)炎性反应的调整作用。方法:将70只昆明小鼠随机分为7个组:LP高剂量组(LP-H)、LP中剂量组(LP-M)、LP低剂量组(LP-L),此三组分别于尾静脉注射LP 50、25、10 mg/kg和LPS 3 mg/kg;依诺肝素组(依诺肝素2 IU/kg+LPS3 mg/kg),模型组(LPS 3 mg/kg),LP对照组(LP 50 mg/kg),空白对照组(生理盐水)。检测小鼠肛温;ELISA法测定小鼠血清白细胞介素1β(IL-1β)、白细胞介素8(IL-8)、肿瘤坏死因子-α(TNF-α)、一氧化氮(NO)、前列环素(PGI2)含量;RT-PCR法测定主动脉内皮型一氧化氮合酶(e NOS)、诱导型一氧化氮合酶(i NOS)、环氧合酶-2(COX-2)m RNA的表达。结果:LP能够降低LPS炎症小鼠体温(P<0.05),降低血清IL-1β、IL-8、TNF-a、NO、PGI2水平(P<0.05-0.01);上调e NOS m RNA表达(P<0.01);下调i NOS m RNA、COX-2 m RNA表达(P<0.01)。结论:LP在LPS炎性反应中抑制炎症因子产生,调整内皮相关基因的表达。 Objective:To investigate the effect of Laminaria Polysaecharide(LP)on inflammatory stress induced by lipopolysaccharide(LPS)in vascular endothelial cells(VECs). Methods:70 Kunming mice were divided into 7 groups randomly:high dose LP group(H-LP),middle dose LP group(M-LP),low dose LP group(L-LP),those were treated with LP 50、25、10 mg/kg and LPS 3 mg/kg from tail vein;enoxaparin group(enoxaparin 2 IU/kg + LPS 3 mg/kg),model group(LPS 3 mg/kg),LP control group(LP 50 mg/kg),saline control group(physiological saline). Rectal temperature in mice was measured. Serum level of IL-1β,IL-8,TNF-α,NO,6-keto-PGF1α were measured by ELISA;The expressions of i NOS m RNA,e NOS m RNA and COX-2 m RNA in aorta were detected by RT-PCR. Results:LP can decrease body temperature of LPS inflammatory mice;reduce the Serum level of IL-1β,IL-8,TNF-α,NO,6-ketoPGF1α(P0.05-0.01);up-regulate the expression of e NOS m RNA(P0.01),down-regulate the expression of i NOS m RNA and COX-2 m RNA(P0.01). Conclusion:LP inhibits Inflammatory factors production,adjusts the expression of endothelium related genes in LPS induced inflammatory stress.
出处 《岭南急诊医学杂志》 2017年第6期513-516,共4页 Lingnan Journal of Emergency Medicine
基金 国家自然科学基金(81660312) 广西自然科学基金(2015GXNSFAA139148)
关键词 海带多糖 脂多糖 血管内皮细胞 炎症因子 laminaria polysaccharide lipopolysaccharide vascular endothelial cells inflammatory factors
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