ABSTRACT
Objective To observe the effects of Soyasaponins on inflammatory factors, antioxidant activity and exercise ability in rats with severe heat stroke. Methods Eighty male Sprague-Dawley (SD) rats were randomly divided into normal control group, heat shock model group, saline control group and Soyasaponin group, The rats that died during the experiment or with a low rectal temperature (< 41℃) were excluded, and finally 54 rats were included, 18 rats remaining in each group. The rats in the heat shock model group were placed in the simulated hot climate animal cabin at 30 ℃, and the temperature within 30 minutes was raised to 39 ℃ in the cabin with 65% humidity; in the mean time, the rat models of heat shock were replicated under the following situations: let the rats exercise on a treadmill with running speed set at 15 m/min, slope degree 0°, once running for 8 minutes, interval 2 minutes and the heat shock time was 90 minutes, the rats in the normal control group were fed in an environment with temperature ranging from 23-25 ℃ and relative humidity ranging from 50%-70%. After the establishment of models, the saline control group and Soyasaponin group were given daily saline and Soyasaponin (10 mg/kg) respectively by gavage for 3 consecutive months, while the heat shock model group was not given any treatment. The femoral artery blood was collected 24 hours after the rats left the cabin. The serum levels of interleukins (IL-6, IL-1β), tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), malonaldehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) were measured by enzyme-linked immunosorbent (ELISA) and the contents of serum hemoglobin (Hb), serum urea (BUN), lactate dehydrogenase (LDH) and blood lactic acid (Lac) were measured by automatie biochemical analyzer. Results The levels of IL-6, IL-1β, TNF-α, IFN-γ, MDA, Hb, BUN, LDH, Lac in heat shock model group were significantly higher than those of the normal control group [IL-6 (ng/L): 86.17±4.82 vs. 12.60±3.49, IL-1β (ng/L): 83.00±5.98 vs. 15.70±3.64, TNF-α (ng/L): 72.22±6.93 vs. 13.75±2.69, IFN-γ (ng/L): 36.22±3.02 vs. 7.35±1.60, MDA (nmol/mg): 19.78±4.56 vs. 6.40±1.35, Hb (g/L): 136.22±1.93 vs. 126.75±5.84, BUN (mmol/L):21.06±3.44 vs. 5.65±1.35, LDH (μmoL·s-1·L-1): 9.65±0.83 vs. 2.12±0.17, Lac (mmol/L): 552.56±78.33 vs. 1.32±0.18, all P ＜ 0.05], SOD and GSH-Px were significantly lower than those in normal control group [SOD (kU/L):97.89±10.57 vs. 126.65±11.35, GSH-Px (kU/L): 19.22±2.58 vs. 43.45±4.02]; however, the levels of IL-6, IL-1β, TNF-α, IFN-γ, MDA, BUN, LDH and Lac in Soyasaponin group were significantly lower than those in heat shock model group [IL-6 (ng/L): 45.28±3.54 vs. 86.17±4.82, IL-1β (ng/L): 41.61±2.93 vs. 83.00±5.98, TNF-α (ng/L):37.22±2.46 vs. 72.22±6.93, IFN-γ (ng/L): 19.22±2.60 vs. 36.22±3.02, MDA (nmol/mg): 11.28±1.74 vs. 19.78±4.56, BUN (mmol/L): 11.78±2.13 vs. 21.06±3.44, LDH (μmoL·s-1·L-1): 3.70±0.26 vs. 9.65±0.83, Lac (mmol/L): 274.56±59.08 vs. 552.56±78.33, all P < 0.01], SOD, GSH-Px and Hb were significantly higher than those of heat shock model group [SOD (kU/L): 116.11±11.28 vs. 97.89±10.57, GSH-Px (kU/L): 31.17±2.90 vs. 19.22±2.58, Hb (g/L): 141.33±3.79 vs. 136.22±1.93, all P < 0.01]; there were no significant statistical differences in above indexes between heat shock model group and saline control group (all P > 0.05). Conclusion After heat shock and exercise management, the production and release of inflammatory factors are increased, and the level of lipid peroxidation was elevated in rats. The Soyasaponin can improve the ability to withstand heat shock and strong exercise by reducing the production and release of inflammatory factors and lipid peroxidation in the rats with severe heatstroke.
ABSTRACT
Objective To observe the effect of different core temperatures (Tc) after heat strike on serum inflammatory cytokines and multiple organ dysfunction syndrome (MODS) in rat. Methods 120 male Sprague-Dawley (SD) rats were randomly divided into normal control group (n = 30) and heat strike group (n = 90). The rats in heat strike group were put into simulated thermal climate animal module after adaptive training. The module temperature was raised to 39 ℃ in 30 minutes with 65% humidity. The rats ran simultaneously at 15 m/min, on the slope of 0°, 8 minutes each time, 2 minutes interval, and the heat strike time was 90 minutes. After the rats came out of the module, rectal temperature, which was Tc value, was recorded. The rats died or Tc < 41 ℃ during the experiment were excluded, the remaining 73 rats were divided into three subgroups: 41.0-41.9 ℃ (n = 38), 42.0-42.9 ℃ (n = 26), and ≥43.0 ℃ (n = 9). The rats in the normal control group were reared at temperature of (25±2) ℃, and humidity of (55±5)%. At 0 hour and 24 hours after the rats came out of the module, femoral artery blood was collected to determine serum interleukins (IL-1α, IL-1β, IL-17), tumor necrosis factor-α(TNF-α) andγ-interferon (IFN-γ) by enzyme-linked immunosorbent assay (ELISA). The cardiac troponin I (cTnI), MB isoenzyme of creatine kinase (CK-MB), serum creatinine (SCr), blood urea nitrogen (BUN), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) levels were determined by automatic biochemical analyzer. The incidence of MODS and the number of accumulative organs within 24 hours of the rats in different Tc of heat strike group were compared and analyzed. Results The serum inflammatory cytokines and biochemical parameters at 0 hour after heat strike were significant higher than those of the normal control group, and showed a time dependence. Further analysis showed that the inflammatory response and organ dysfunction in rats were increased gradually with the increase in Tc of rats. Compared with the normal control group, at 24 hours after heat strike, inflammatory cytokines in Tc≥43.0 ℃ rats were increased obviously [IL-1α (ng/L): 13.56±2.07 vs. 2.24±0.62, IL-1β (ng/L): 17.11±1.90 vs. 7.40±1.52, IL-17 (ng/L): 17.00±1.41 vs. 6.00±1.78, TNF-α (ng/L):16.78±1.79 vs. 7.27±1.74, IFN-γ (ng/L): 21.11±2.09 vs. 10.43±2.31], and the biochemical parameters were also increased obviously [cTnI (ng/L): 50.78±6.67 vs. 20.53±3.09, CK-MB (U/L): 62.89±3.82 vs. 22.00±3.01, SCr (μmol/L): 149.22±4.35 vs. 92.53±8.32, BUN (nmol/L): 55.22±1.99 vs. 19.10±2.02, ALT (U/L): 388.33±4.97 vs. 100.23±10.61, AST (U/L): 361.22±6.53 vs. 97.67±10.54, all P < 0.01]. The incidence of MODS within 24 hours in the heat strike group was 54.79% (40/73), and the higher the Tc, the higher the incidence of MODS, and the more insulted organs [the incidence of MODS in 41.0-41.9 ℃, 42.0-42.9 ℃, and ≥43.0 ℃ subgroups was 36.84% (14/38), 65.38% (17/26), 100.00% (9/9), and the organ involvement rate was 12.17% (37/304), 23.08% (48/208), and 48.61% (35/72), respectively, when 8 organs or systems were calculated for each rat, both P < 0.01]. Conclusion The higher the Tc of heat strike rats, the stronger the inflammatory reaction and the more serious the damage of tissue, and the more extensive damage of the organs.
ABSTRACT
Objective To investigate the protective effect of mild hypothermia at different starting times on the physiological functions of the viscera of exertional heat stroke (EHS). Methods A prospective randomized controlled trial was conducted. EHS patients admitted to intensive care unit of the 159th Hospital of People's Liberation Army and the First Affiliated Hospital of Zhengzhou University from June 2015 to June 2017 were enrolled. The patients were divided into 2, 4, 6 hours start hypothermia treatment groups according to the random number table method, the mild hypothermia was initiated at 2, 4 and 6 hours after the disease onset respectively, and the methods were the same in each group. After treatment of 2, 12, 24 hours, the venous blood in the three groups was collected to detect serum cardiac troponin I (cTnI) with chemiluminescence method, MB isoenzyme of creatine kinase (CK-MB) with immunosuppressive method, creatinine (Cr) with creatine oxidase method, β2-microglobulin (β2-MG) with turbidimetry, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) with enzyme method. Multiple organ dysfunction syndrome (MODS) within 24 hours after treatment was recorded. Linear regression analysis of the correlation between mild hypothermia start-up time and MODS was done. Results Ninety-three cases of EHS were included,with 32, 31 and 30 patients in 2, 4, 6 hours start treatment groups respectively. There were no significant differences in gender, age, core temperature, onset time to admission, Glasgow coma scale (GCS), acute physiology and chronic health evaluation system Ⅱ(APACHE Ⅱ) score at admission among the three groups. There were no significant differences in the levels of serum cTnI, CK-MB, Cr, β2-MG, ALT and AST at 2 hours after treatment. But with the prolongation of the treatment time, all indicators gradually increased. And the earlier start of the mild hypothermia, the less significant of the above indexes. All indexes in 2 hours start treatment group were significantly lower than those of 2 hours and 6 hours start treatment groups at 24 hours after treatment [cTnI (ng/L): 49.53±9.25 vs. 56.52±10.05, 64.57±11.21; CK-MB (U/L):51.47±11.83 vs. 57.87±7.43, 64.40±7.93; Cr (μmol/L): 140.97±11.33 vs. 148.16±10.39,155.57±8.65; β2-MG (mg/L): 10.28±1.46 vs. 11.58±2.13, 12.93±1.98; ALT (U/L): 248.53±75.47 vs. 341.42±129.58, 425.77±101.23;AST (U/L): 197.25±42.59 vs. 292.81±58.49, 351.20±60.41, all P < 0.05]. There was significant difference in the incidence of MODS in 2, 4, 6 hours start treatment groups [43.75% (14/32), 64.52% (20/31), 80.08% (24/30), χ2= 8.761, P = 0.013]. Linear regression analysis showed that the earlier onset time of mild hypothermia, the lower incidence of MODS (R2= 0.915, P = 0.013). Conclusion The application of mild hypothermia in 2 hours can effectively protect the physiological function of EHS organs and reduce the incidence of MODS.