Xuebijing injection reduces organ injuries and improves survival by attenuating inflammatory responses and endothelial injury in heatstroke mice.

Xuebijing injection reduces organ injuries and improves survival by attenuating inflammatory responses and endothelial injury in heatstroke mice.
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血必净注射液通过减轻中暑小鼠的炎症反应和内皮损伤来减少器官损伤并提高生存率。

DOI:
10.1186/s12906-015-0519-5
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发表时间:
2015-02-05
影响因子:
--
通讯作者:
Su L
Su L
中科院分区:
医学3区
文献类型:
--
作者:
Xu Q;Liu J;Guo X;Tang Y;Zhou G;Liu Y;Huang Q;Geng Y;Liu Z;Su L

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中暑的发病机制是一个多因素的过程,涉及随后的炎症,内皮损伤和凝血功能障碍之间的相互作用,这使得中暑的药物治疗成为一个具有挑战性的问题。血必净注射液是一种治疗脓毒症的传统中药,有报道可抑制炎症反应和恢复凝血功能障碍。然而,人们对XBJ在中暑中的作用知之甚少。在诱导中暑之前和/或之后用指定剂量的XBJ处理小鼠。ELISA法检测血清炎症因子肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)及内皮标志物血管性血友病因子(vWF)、E-选择素。通过UniCel DxC 800 Synchron临床系统评价肝脏、肾脏和心脏特征,包括丙氨酸氨基转移酶、天冬氨酸氨基转移酶、肌酐、血尿素氮和乳酸脱氢酶,并通过ELISA测定肌钙蛋白。使用STA Compact®止血系统检查凝血特征,包括凝血酶时间、凝血酶原时间、活化部分凝血活酶时间、国际标准化比率和纤维蛋白原。H&E染色评价空肠损伤。电镜观察心肌线粒体结构的变化。血必净预处理可剂量依赖性地降低中暑小鼠血清促炎细胞因子TNF-α和IL-6以及内皮损伤标志物vWF和E-selectin的水平。当在热损伤之后或之前和之后给予XBJ时,观察到类似的保护作用。这些保护作用持续超过12小时,在小鼠接受XBJ之前和之后的热损伤。XBJ还提高了中暑小鼠的存活率,改善了肝脏,心脏和肾脏损伤,包括心脏线粒体损伤,并减少了凝血障碍。XBJ通过减轻炎症反应和内皮损伤来预防中暑小鼠的器官损伤并提高存活率。因此,血必净可能是一种潜在的预防和治疗中暑的有效药物.
The pathogenesis of heatstroke is a multi-factorial process involved with an interplay among subsequent inflammation, endothelial injury and coagulation disturbances, which makes pharmacological therapy of heatstroke a challenging problem. Xuebijing injection (XBJ), a traditional Chinese medicine used to sepsis, has been reported to suppress inflammatory responses and restore coagulation disturbances. However, little is known about the role of XBJ in heatstroke. Mice were treated with indicated dose of XBJ before and/or after the induction of heatstroke. Serum inflammatory cytokines, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), and endothelial markers, von Willebrand Factor (vWF) and E-selectin, were measured by ELISA. Liver, kidney and heart profiles including alanine aminotransferase, aspartic aminotransferase, creatinine, blood urea nitrogen, and lactate dehydrogenase, were evaluated by UniCel DxC 800 Synchron Clinical Systems, and troponin was measured by ELISA. Coagulation profiles, including thrombin time, prothrombin time, activated partial thromboplastin time, international normalized ratio, and fibrinogen were examined by STA Compact® Hemostasis System. Jejunum injury was evaluated with H&E staining. Changes in mitochondrial structure in cardiac tissue were assesed by electron microscopy. Pretreatment with XBJ decreased serum pro-inflammatory cytokines including TNF-α and IL-6, as well as endothelial injury markers, vWF and E-selectin, in a dose-dependent manner in heatstroke mice. Similar protective effects were observed when XBJ was administered after, or both before and after heat insult. These protective effects lasted for over 12 h in mice receiving XBJ before and after heat insult. XBJ also improved survival rates in heatstroke mice, ameliorated liver, heart, and kidney injuries, including mitochondrial damage to the heart, and reduced coagulation disturbances. XBJ prevents organ injuries and improves survival in heatstroke mice by attenuating inflammatory responses and endothelial injury. XBJ may be a potentially useful in the prevention and treatment of heatstroke.
DOI: 10.1161/atvbaha.107.158709
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