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

被引：51

作者：

Chen, Yi ^{[1
]}

Tong, Huasheng ^{[2
]}

Pan, Zhiguo ^{[2
]}

Jiang, Dongxin ^{[1
]}

Zhang, Xinqin ^{[2
]}

Qiu, Junming ^{[2
]}

Su, Lei ^{[2
]}

Zhang, Minzhou ^{[3
]}

机构：

[1] Jinan Univ, Affiliated Med Coll, Peoples Hosp Dongguan 5, Dept Crit Care Med, Dongguan 523900, Guangdong, Peoples R China

[2] Guangzhou Gen Hosp Guangzhou Mil Command, Key Lab Trop Trauma Care & Tissue Repair PLA, Dept Crit Care Med, 111 Liuhua Rd, Guangzhou 515000, Guangdong, Peoples R China

[3] Guangdong Hosp Tradit Chinese Med, Dept Crit Care Med, 111 Dade Rd, Guangzhou 510120, Guangdong, Peoples R China

来源：

EXPERIMENTAL AND THERAPEUTIC MEDICINE | 2017年 / 13卷 / 06期

基金：

中国国家自然科学基金;

关键词：

Xuebijing injection; heat stroke; pulmonary injury; oxidative stress; inflammation; apoptosis; ACUTE LUNG INJURY; ACTIVATED PROTEIN-C; EXPERIMENTAL HEATSTROKE; INFLAMMATION; DYSFUNCTION; RESPONSES; CYTOKINE; THERAPY; CELLS; MODEL;

D O I：

10.3892/etm.2017.4444

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

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, 54rats 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 60min. The concentration of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta) 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-alpha, IL-1 beta 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.

引用

页码：3408 / 3416

页数：9

共 37 条

[1] Experimental heatstroke in baboon: Analysis of the systemic inflammatory response [J].