Xuebijing injection attenuates pulmonary injury by reducing oxidative stress and proinflammatory damage in rats with heat stroke.

Xuebijing injection attenuates pulmonary injury by reducing oxidative stress and proinflammatory damage in rats with heat stroke.
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血必净注射液通过减少中暑大鼠氧化应激和促炎性损伤减轻肺损伤

DOI:
10.3892/etm.2017.4444
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发表时间:
2017-06
影响因子:
2.7
通讯作者:
Zhang M
Zhang M
中科院分区:
医学4区
文献类型:
--
作者:
Chen Y;Tong H;Pan Z;Jiang D;Zhang X;Qiu J;Su L;Zhang M

文献摘要

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本研究旨在探讨血必净注射液对中暑大鼠肺损伤的保护作用及其机制。总共有54只大鼠被随机分配到非热、盐水溶剂和XBJ组。记录大鼠直肠温度(Tc)、平均动脉压(MAP)和呼吸频率(RR)。观察中暑时间点和生存时间,并于0~60 min内定期检测动脉血气指标,同时检测肿瘤坏死因子-α(TNF-α)、白细胞介素-1 β(IL-1 β)和IL-10的浓度。在实验结束时,收获肺组织用于组织病理学分析。免疫组化法检测诱导型一氧化氮合酶(iNOS)和超氧化物歧化酶(SOD)的表达。末端脱氧核苷酸转移酶介导的dUTP缺口末端标记用于测量细胞凋亡。热应激大鼠Tc、MAP、RR及动脉血气指标升高,表明XBJ预处理延长了热应激大鼠临床特征的下降。生理盐水组大鼠的中暑时间和存活时间均短于XBJ组。生理盐水组大鼠肺组织iNOS表达及支气管肺泡灌洗液中TNF-α、IL-1 β、IL-10浓度均高于血必净预处理组。生理盐水组SOD的表达明显低于血必净组。生理盐水组大鼠肺组织细胞凋亡率明显高于血必净组。结论:XBJ可通过改善肺功能衰竭和急性肺损伤,延缓中暑的发生,延长热应激大鼠的生存时间。其作用机制可能是通过减少炎症细胞因子、减轻氧化应激和细胞凋亡而实现的。
The present study aimed to investigate the protective effect of Xuebijing injection (XBJ) on lung injury in heat-stroke rats and the underlying mechanisms. In total, 54 rats were randomly assigned to non-thermal, saline vehicle and XBJ groups. The rectal temperature (Tc), mean arterial pressure (MAP) and respiratory rate (RR) of the rats were recorded. The time-point of heat stroke and the time of survival were assessed, and indicators of arterial blood gas were regularly measured from 0 to 60 min. The concentration of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-10 was also determined. At the end of the experiment, lung tissue was harvested for histopathological analysis. Inducible nitric oxide synthase (iNOS) and superoxide dismutase (SOD) expression was measured by immunohistochemistry. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling was used to measure apoptosis. XBJ pretreatment prolonged the decline of clinical characteristics, as demonstrated by increases in Tc, MAP, RR and indicators in arterial blood gas in rats under heat stress. The time until heat stroke and the survival time in the Saline group were shorter than in rats treated with XBJ. The expression of iNOS in lung tissue and the concentration of TNF-α, IL-1β and IL-10 in the bronchoalveolar lavage fluid of rats treated with saline was higher than in rats with XBJ pre-treatment. Contrarily, SOD expression in rats treated with saline was decreased compared with that in rats treated with XBJ. Moreover, the apoptotic rate in the lung tissues of rats with saline treatment was higher than that in rats treated with XBJ. In conclusion, XBJ delayed the development of heat stroke and increased the survival time in rats under heat-stress by ameliorating pulmonary failure and acute lung injury. The underlying mechanisms of this effect may be the reduction of inflammatory cytokines as well as attenuation of oxidative stress and apoptosis by XBJ.