Abstract
This study aimed to investigate the protective mechanism of Xuebijing injection (XBJ) against heat stroke (HS) in rats. Adult male Sprague Dawley rats were randomly divided into normal control (NC), normal saline-treated HS (NS-HS) and XBJ-treated HS (XBJ-HS) groups. At 47 and 57 min from the initiation of heat stress (42.5–43.5°C), the plasma levels of certain cytokines [interleukin (IL)-1β, IL-6 and tumor necrosis factor-α], biochemical indicators (creatinine, blood urea nitrogen, aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase) and coagulation indicators (activated partial thromboplastin time, prothrombin time, fibrinogen degradation products and D-dimer) were detected, and microscopy of the liver tissue of the rats was conducted. At 47 and 57 min after the initiation of the heat stress, the levels of the cytokines, coagulation indicators and biochemical indicators in the NS-HS group were significantly higher than those in the NC group (P<0.05). In the NS-HS group, the levels of the aforementioned indices were significantly reduced compared with those in the NC and NS-HS groups (P<0.05). In the NS-HS group, serious liver cell congestion, nuclear swelling and central vein dilation were visible, along with the appearance of bubbles in the liver tissue. In the XBJ-HS group, only a small number of congestive liver cells were identified, with occasional nuclear swelling but no bubbles, which was similar to the observations in the NC group. Early intervention treatment of HS with XBJ is able to reduce the systemic inflammatory response and coagulation activity and decrease the tissue ischemia and injury degree, thus extending the survival time of rats with HS.
Highlights
Heat stroke (HS) is a type of nerve damage caused by thermoregulatory dysfunction and excessive accumulation of body heat due to high temperature
Xuebijing injection (XBJ) was purchased from Tianjin Hongri Pharmaceutical Stock Co., Ltd. (Tianjin, China). [125I]‐labeled tumor necrosis factor‐α (TNF‐α), interleukin (IL)‐1β and IL‐6 radioimmunoassay kits were provided by Beijing North Institute of Biological Technology (Beijing, China)
In the subsequent 10 min it declined to 136 mmHg, with a descent of 24 mmHg from the peak which indicated the occurrence of HS
Summary
Heat stroke (HS) is a type of nerve damage caused by thermoregulatory dysfunction and excessive accumulation of body heat due to high temperature. HS is the most severe form of heat stress, with extensive damage to the body, and may lead to functional and morphological changes of numerous organs and systems. Cytokines may mediate the systemic inflammatory response, and play key roles in the process of HS [4]. The uncontrolled systemic inflammatory response causes a cascade resulting in multiple organ dysfunction syndrome (MODS). Bouchama and Knochel [1] consider that the characteristic pathological and clinical manifestations of HS are the interaction results of complex physiological and biochemical mechanisms prior to body collapse, including thermoregulatory imbalance, enlargement of the acute‐phase response and the expression of heat shock protein (HSP)
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