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羟基红花黄色素 A 可减轻急性软组织损伤中炎症细胞因子的表达。

Hydroxysafflor yellow A attenuates the expression of inflammatory cytokines in acute soft tissue injury.

机构信息

Department of Pharmacology, Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart Lung and Blood Vessel Disease, Beijing, P.R. China.

出版信息

Sci Rep. 2017 Jan 11;7:40584. doi: 10.1038/srep40584.

DOI:10.1038/srep40584
PMID:28074914
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5225459/
Abstract

We examined the effect of hydroxysafflor yellow A (HSYA) on the inflammatory response to strike-induced acute soft tissue injury in rats. Soft tissue injury was induced in rat leg muscles using a strike hammer, followed by intraperitoneal administration of HSYA at 16, 32, or 64 mg/kg. After 24 h, the rats were anaesthetized, blood and muscle samples were taken. Plasma levels of interleukin (IL)-6, IL-1β, and tumour necrosis factor (TNF)-αwere measured by enzyme-linked immunosorbent assay. Total RNA and protein were isolated from muscle tissue to determine the mRNA levels of IL-6, IL-1β, TNF-α, vascular cell adhesion molecule (VCAM)-1, and intercellular adhesion molecule (ICAM)-1, and the protein level of phosphorylated p38 mitogen-activated protein kinase (MAPK). Nuclear factor (NF)-κB expression was determined by muscle histopathology and immunohistochemistry. HSYA attenuated pathologic changes instrike-induced soft tissue inflammation. Treatment with HSYA also alleviated strike-induced increases in TNF-α, IL-1β, IL-6, VCAM-1, and ICAM-1mRNA levels and inhibited the increased activation of NF-κB and phosphorylation of p38 MAPK in muscle tissue. These findings suggest that HSYA effectively inhibits strike-induced inflammatory signal transduction in rats.

摘要

我们研究了羟基红花黄色素 A(HSYA)对打击诱导的急性软组织损伤大鼠炎症反应的影响。使用打击锤在大鼠腿部肌肉中诱导软组织损伤,然后腹膜内给予 HSYA 16、32 或 64mg/kg。24 小时后,麻醉大鼠,取血和肌肉样本。通过酶联免疫吸附试验测量血浆中白细胞介素(IL)-6、IL-1β和肿瘤坏死因子(TNF)-α的水平。从肌肉组织中分离总 RNA 和蛋白质,以确定 IL-6、IL-1β、TNF-α、血管细胞黏附分子(VCAM)-1 和细胞间黏附分子(ICAM)-1 的 mRNA 水平,以及磷酸化 p38 丝裂原活化蛋白激酶(p38 MAPK)的蛋白水平。通过肌肉组织病理学和免疫组织化学测定核因子(NF)-κB 的表达。HSYA 减轻了打击诱导的软组织炎症的病理变化。HSYA 治疗还减轻了打击引起的 TNF-α、IL-1β、IL-6、VCAM-1 和 ICAM-1mRNA 水平的增加,并抑制了肌肉组织中 NF-κB 的增加激活和 p38 MAPK 的磷酸化。这些发现表明 HSYA 可有效抑制大鼠打击诱导的炎症信号转导。

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