Green tea polyphenol epigallocatechin-3-gallate ameliorates insulin resistance in non-alcoholic fatty liver disease mice.

AIM: Epigallocatechin-3-gallate (EGCG) is a major polyphenol in green tea. In this study, we investigated the effects of EGCG on insulin resistance and insulin clearance in non-alcoholic fatty liver disease (NAFLD) mice. METHODS: Mice were fed on a high-fat diet for 24 weeks. During the last 4 weeks, the mice were injected with EGCG (10, 20 and 40 mg·kg(-1)·d(-1), ip). Glucose tolerance, insulin tolerance and insulin clearance were assessed. After the mice were euthanized, blood samples and tissue specimens were collected. Glucose-stimulated insulin secretion was examined in isolated pancreatic islets. The progression of NAFLD was evaluated histologically and by measuring lipid contents. Insulin-degrading enzyme (IDE) protein expression and enzyme activity were detected using Western blot and immunocapture activity assays, respectively. RESULTS: The high-fat diet significantly increased the body weight and induced grade 2 or 3 liver fatty degeneration (steatosis, lobular inflammation and ballooning) accompanied by severe hyperlipidemia, hyperglycemia, hyperinsulinemia and insulin resistance in the model mice. Administration of EGCG dose-dependently ameliorated the hepatic morphology and function, reduced the body weight, and alleviated hyperlipidemia, hyperglycemia, hyperinsulinemia and insulin resistance in NAFLD mice. Furthermore, EGCG dose-dependently enhanced insulin clearance and upregulated IDE protein expression and enzyme activity in the liver of NAFLD mice. CONCLUSION: EGCG dose-dependently improves insulin resistance in NAFLD mice not only by reducing body weight but also through enhancing the insulin clearance by hepatic IDE. The results suggest that IDE be a potential drug target for the treatment of NAFLD.

Effects and mechanisms of vitamin A and vitamin E on the levels of serum leptin and other related cytokines in rats with rheumatoid arthritis.

Leptin has been identified as an important cytokine in the inflammatory networks of rheumatoid arthritis (RA). Higher serum leptin levels may accelerate the development of RA. This study aimed to examine the effects of vitamin A (VitA) and vitamin E (VitE) on the levels of leptin and other related experimental and clinical indices, and to explore the mechanisms of these effects through the Janus kinase/signal transducer and activator of transcription (STAT) signal transduction pathway in rats with collagen-induced arthritis (CIA). CIA model rats were established by the intradermal injection of bovine type II collagen emulsified in incomplete Freund's adjuvant, followed by a booster intradermal injection. Four weeks later, the CIA model rats were treated with 42.86 µg retinol equivalents/kg body weight (b.w.) VitA or 200 mg/kg b.w. VitE for four weeks. The levels of leptin, tumor necrosis factor-α (TNF-α), interleukin (IL)-6, IL-10, IL-4, C-reactive protein (CRP) and rheumatic factor were measured by ELISA using commercial kits, and the erythrocyte sedimentation rate (ESR) was determined. In addition, the expression levels of phosphorylated (p)-STAT1, p-STAT3 and leptin in the synovium were evaluated by western blot analysis. The results indicated that VitA and VitE significantly reduced the levels of leptin, TNF-α, IL-6 and CRP and the ESR and significantly increased the levels of IL-10 compared with those of the model group. Furthermore, significantly reduced p-STAT3 protein expression levels were observed in the VitA and VitE groups. In conclusion, VitA and VitE reduced the levels of serum leptin protein and other cytokines. Furthermore, VitA and VitE also reduced the p-STAT3 protein levels. The present study may provide a novel approach for the treatment of RA.

Protective mechanism of andrographolide against carbon tetrachloride-induced acute liver injury in mice.

The aim of this study was to investigate the protective effects of andrographolide (AP), a bioactive component isolated from Andrographis paniculata, on carbon tetrachloride (CCl(4))-induced liver injury as well as the possible mechanisms involved in this protection in mice. Acute liver injury was induced by CCl(4) intoxication in mice. Serum biological analysis, lipid peroxides and antioxidant estimation, histopathological studies, reverse transcription polymerase chain reaction (RT-PCR) and Western blot assay were carried out. CCl(4) treatment resulted in severe hepatic injury, as evidenced by significant elevation of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels and typical histopathological changes, such as hepatocyte necrosis. Additionally, CCl(4) administration led to oxidative stress in mice, as indicated by a remarkable increase in the hepatic malondialdehyde (MDA) level, together with a significant decrease in liver reduced glutathione (GSH) content. However, CCl(4)-induced hepatotoxicity was significantly attenuated by pretreatment with AP, as demonstrated by significant reduction of serum ALT, AST levels and hepatic MDA activity, along with a remarkable increase in hepatic GSH content. Histopathological changes induced by CCl(4) were also ameliorated by AP pretreatment. The marked increase of tumor necrosis factor-α (TNF-α) induced by CCl(4) was attenuated by AP, and the dramatic elevation of heme oxygenase-1 (HO-1) at transcriptional and protein levels was augmented following AP pretreatment. AP can effectively prevent liver injury induced by CCl(4), which may be due to inhibition of oxidative stress and inflammatory responses.

[Protective effects of nerve growth factor vs Danshen on hippocampal neuron against global ischemia-reperfusion injury in gerbils].

OBJECTIVE: To study the protective effects of nerve growth factor (NGF) and Danshen on hippocampal neurons in gerbils (Meriones unguiculatus) with global ischemia-reperfusion injury. METHODS: Global ischemia-reperfusion model was established in 54 male Z:ZCLA gerbils by occlusion of the bilateral carotid arteries. The animal models were randomized into 3 groups to receive treatment with normal saline, NGF, and Danshen 30 min after the reperfusion. At 6 h, 3 and 7 days after the reperfusion, the survival of the hippocampal CA1 pyramidal neurons was observed using optical and electron microscopy, and immunohistochemistry was employed to detect the expressions of Bcl-2 and Bax in the neurons. RESULTS: Neuronal apoptosis was not observed in the hippocampus 6 h after the reperfusion, but at 3 and 7 days, the number of apoptotic neurons increased significantly in the CA1 region. Compared with normal saline, treatments with NGF and Danshen both significantly reduced the number of apoptotic neurons at 3 and 7 days. The number of apoptotic neurons showed no significant difference between NGF and Danshen treatment groups at 3 days, but at 7 days, the apoptotic cell number was significantly lower in NGF group (P<0.05). Bcl-2 expression was the highest in NGF group, and its highest expression occurred at 6 h after the reperfusion; Bax expression was detected in saline group, and underwent no significant changes with the passage of time. CONCLUSION: Both NGF and Danshen show protective effects against global ischemia-reperfusion injury. NGF has a stronger protective effect than Danshen, and this finding provides experimental evidence for selecting appropriate protective agents in the treatment of ischemic brain damage.

[Construction of MHV-A59 damp-heat mouse model and analysis of the relevant indices].

OBJECTIVE: To explore the impact of inflammation, water metabolism and immune function on the establishment of a mouse model of damp-heat syndrome with MHV-A59 infection. METHODS: Twenty-four mice were randomly divided into control group, virus group, damp-heat group and model group. The peripheral blood CD4(+) and CD8(+) lymphocytes were detected by flow cytometry, and the serum levels of IFN-γ and IL-4 were assayed by ELISA. The expressions of NF-κB and AQP4 in the liver and stomach were determined using immunohistochemistry. RESULTS: The expression of NF-κB and CD4(+)/CD8(+) ratio in the virus and model groups were significantly higher than those in the damp-heat and control groups, while the expression of AQP4 was significantly higher in the model and damp-heat groups than in the other groups. Compared with the control group, the model group showed a significantly higher ratio of IFN-γ/IL-4. CONCLUSIONS: MHV-A59 virus is the main cause of elevated NF-κB expression and CD4(+)/CD8(+)/ ratio, while damp-heat syndrome is responsible for increased AQP4 expression, and their synergistic effect results in increased IFN-γ/IL-4 ratio. The mouse model established using MHV-A59 virus and the damp-heat factors can mimic damp-heat syndrome described in traditional Chinese medicine theory.

[The mechanism of signal extension in Haoqin Qingdan decoction immunity activity in Damp-heat syndrome of pneumonia disease infected by influenza virus].

OBJECTIVE: To explore the immunoregulation existing signal transduction mechanism, to evaluate the role of lay its experimental basis By using Haoqin Qingdan decoction for treatments on the mouse models. METHODS: A total of 40 NIH Mice were randomly divided into five groups: control group, virus group (infecting by influenza virus), complex model group (richly fatty and sweet diet + Humid heat environment + infecting by influenza virus), virazole group (mouse of model group was treated by virazole), and Haoqin Qingdan decoction group (mouse of complex model group was treated by decoction of Haoqin Qingdan). When the complex model was established, determination of the mice lung indexes in each group and calculate the inhibition of lung indexes. The level of TLR2 mRNA and NF-κB mRNA expressions of peritoneal macrophages in each group of mice were quantitated by reverse transcription-polymerase chain reaction (RT-PCR). The level of IL-4 and IFN-γ in mouse serum was detected by ELISA to calculate the Th1/Th2 (IFN-γ/IL-4). RESULTS: The lung index of control group, virus group, complex model group, virazole group and Haoqin Qingdan decoction group were separately: (0.79 ± 0.11)%, (1.93 ± 0.38)%, (1.41 ± 0.26)%, (1.10 ± 0.26)% and (1.02 ± 0.16)%; The mice of virazole group and Haoqin Qingdan decoction group lung index were decreased (t = 0.322, P < 0.05). TLR2 mRNA expression The results showed that the control group, virus group, complex model group, virazole group and Haoqin Qingdan decoction group were: 0.145 ± 0.017, 0.991 ± 0.149, 0.903 ± 0.124, 0.257 ± 0.03 and 0.413 ± 0.031; Compared to the complex model group, Haoqin Qingdan decoction group and virazole group were decreased (t = 0.422, F = 112.834, P < 0.05). Control group, virus group, complex model group, virazole group and Haoqin Qingdan decoction group NF-κB mRNA expression were separately: 0.075 ± 0.148, 0.379 ± 0.019, 0.291 ± 0.012, 0.169 ± 0.026 and 0.175 ± 0.033; the expression in virazole group and Haoqin Qingdan decoction group were decreased (t = 0.422, F = 112.834, P < 0.05). The level of IFN-γ in mice serum of control group, virus group, complex model group, virazole group and Haoqin Qingdan decoction group were: (7434.06 ± 323.27) pg/ml, (8679.77 ± 198.70) pg/ml, (8068.78 ± 113.8) pg/ml, (7454.66 ± 301.30) pg/ml and (7484.56 ± 229.85) pg/ml respectively; the IFN-γ level in serum of Haoqin Qingdan decoction group and virazole group were decreased (t = 0.201, F = 5.390, P < 0.05). Each group of mice IL-4 contents were (3701.74 ± 256.00) pg/ml, (3569.64 ± 161.35) pg/ml, (3530.88 ± 334.63) pg/ml, (3481.84 ± 282.25) pg/ml and (3618.00 ± 262.16) pg/ml; there were no significant difference between each group (t = 0.414, F = 0.505, P > 0.05). Th1/Th2 type cells in state of equilibrium (means IFN-γ/IL-4) were: 2.02 ± 0.19, 2.38 ± 0.10, 2.36 ± 0.14, 2.22 ± 0.17 and 2.07 ± 0.15; and complex model group Haoqin Qingdan decoction group and virazole group were decreased, and there was no significant difference observed (t = 0.587, F = 3.684, P > 0.05). CONCLUSION: The effect of Haoqin Qingdan decoction on treatment of damp-heat syndrome of pneumonia infected by influenza virus was observed. Through reducing the expressions of TLR2, it decreases the levels of NF-κB mRNA and the proportionality of Th1/Th2 are obviously descend (P < 0.05). Haoqin Qingdan decoction can reduce the lung index and relieve the pathogenic changes.

[Effects of selective iNOS inhibitor aminoguanidine on waveform of blood pressure in rat heat stroke].

OBJECTIVE: To evaluate the change of blood pressure, ECG and nitric oxide (NO) in rat heat stroke and effects of aminoguanidine (AG) against heatstroke. METHODS: The male SD rats were randomly assigned into 1 of the following 2 groups: control group or AG group. The rats of control group (n = 10) and AG group (n = 10) were exposed to high ambient temperature (41 degrees C, relative humidity 65%) to induce heatstroke, arterial blood pressures, colonic temperature (T(co)), electrocardiograph (ECG) were monitored. The other rats of both groups (both n = 10) were exposed to high ambient temperature (41 degrees C, relative humidity 65%), and the blood samples were taken at 0, 60 min after the start of heat exposure for determination of the plasma NO concentrations. RESULTS: (1) From 0 min to 50 min after heat exposure, MAPs of two groups were not significantly different, but at about 55 approximately 60 min after the start of heat exposure, MAPs of control group were decreased significantly differently from that of AG group, K value and dicrotic pulse relative height (h(D)/H) were gradually decreased, especially at 40 min after the start of heat exposure, K value of control group decreased significantly comparison with that of AG group; (2) Heart rate (HR) and QT interval of both groups were increased, while PR interval were decreased after the start of heat exposure; (3) T(co) of both groups were increased after the start of heat exposure until T(co) increased to 42 degrees C (the onset of heatstroke), but there was not significantly difference between the two groups; (4) The time of the onset of heatstroke (TOHS) and survival time (ST) of AG group were significantly longer than those of control group; (5) The plasma NO concentrations of the two groups were significantly higher at 60 min than at 0 min after the start of heat exposure, and the plasma NO concentrations of control group were significantly higher than that of AG group at 60 min after the start of heat exposure. CONCLUSION: iNOS may contribute to heatstroke, and aminoguanidine can provide protective effects on heatstroke as a selective iNOS inhibitor.

[Effects of artesunate on CD14 and toll-like receptor 4 in peritoneal macrophages of mice with heat stroke endotoxemia].

OBJECTIVE: To study the effects of artesunate on CD14 and toll-like receptor 4 (TLR 4) expressions in peritoneal macrophages of mice with heat stroke endotoxemia. METHODS: Kunming mice were randomly divided into the normal temperature group, the hyperthermia group, the normal saline (NS) group and the artesunate group (both i.p.60 mg/kg daily for consecutive five days). The normal temperature group was exposed to the condition of dry bulb temperature (Tdb) 25 degrees C +/- 0.5 degrees C and relative humidity (RH) 43% +/- 5% for 2 hours, while other groups were exposed to the condition of Tdb 35 degrees C +/- 0.5 degrees C and RH 65% +/- 5%. The mRNA expressions of CD14 and TLR 4 in peritoneal macrophages and concentrations of tumor necrosis factor alpha (TNF alpha) in plasma were observed in different time points (1 hour and 2 hour). RESULTS: The mRNA expressions of CD14 and TLR 4 in the normal temperature group were 0.34% +/- 0.047% and 0.31% +/- 0.062% respectively. The expressions of two receptors at 1 hour in the hyperthermia group were significantly increased to 0.53% +/- 0.085% and 0.45% +/- 0.049% compared with the normal group and kept increased at 2 hour (P < 0.01). The mRNA expressions at 1 hour in the NS group were significantly increased but a little bit decreased at 2 hour. The mRNA expressions of CD14 and TLR 4 at 1 hour in the artesunate group were 0.26% +/- 0.051% and 0.25% +/- 0.084% respectively and a little bit decreased at 2 hour. The change of TNF-alpha in each group was almost consistent with the changes of CD14 and TLR 4. CONCLUSION: Artesunate can reduce significantly the expressions of CD14 and TLR 4 in LPS signal transduction pathway and the concentration of TNF-alpha, which perhaps is one of the most important mechanisms that artesunate fights against endotoxemia.

[Arterial blood gas analysis in Lipopolysaccharide-heat co-stressed rats].

OBJECTIVE: To observe the change in vital signs and arterial blood gas in Lipopolysaccharide (LPS)-injected heat exposed rats. METHODS: Male pathogen-free Wistar rats were randomly assigned to the following groups: saline-injected normothermic control (C-Group), saline-injected heat exposed (H-Group), LPS-injected normothermic control (L-Group), LPS-injected heat exposed (HL-Group). Rectal temperature (Tr), heart rate (HR), mean arterial pressure (MAP), arterial blood gas were continually monitored. RESULTS: (1) The rats in HL-Group displayed significantly high values of Tr (43.04 degrees C +/- 0.11 degrees C) and HR [(660 +/- 42) beats/min] and low values of MAP [(49.0 +/- 3.5) mm Hg] compared with C-Group. There was a significant difference in the values of Tr, HR, and MAP between HL-Group and L-Group and in the values of HR and MAP between HL-Group and H-Group. (2) The values of PaO(2), HCO(3)(-), PaCO(2) were significantly lower than those in C-Group at 40 min after LPS-injected heat stress. At 120 min, the PaO(2) [(11.59 +/- 1.11) kPa], HCO(3)(-) [(10.42 +/- 1.06) mmol/L], PaCO(2) [(2.82 +/- 0.81) kPa] in HL-Group were significantly lower than those in L-Group. A significant difference in the values of HCO(3)(-) and PaCO(2) between HL-Group and H-Group was also observed. CONCLUSION: LPS-injected heat stress primes the rat to advance and augment the change in vital signs, arterial blood gas, and systemic inflammatory response syndrome.

Protective and anti-fatigue effects of aspirin against heatstroke in rats.

The purpose of this study is to determine whether aspirin can reduce interleukin-1beta(IL-1beta) concentration and exert protective effects against heatstroke. The heatstroke rat model was established through exposing rat to a high ambient temperature (HAT, Ta 41 degrees C, relative humidity 65%) in a simulative HAT chamber to induce heatstroke. Three parts were performed in the present experiment: (1) To determine the effects of pretreatment with aspirin against heatstroke;(2) To prove the effects of specifically reducing inducible nitric oxide synthase (iNOS) against rat heatstroke by iNOS selective prohibitor aminoguanidine (AG);(3) To determine the effects of aspirin against heatstroke and fatigue. In part 1 and 2, Sprague-Dawley rats were randomly assigned to control and aspirin groups or AG groups respectively. Mean arterial blood pressure (MAP), colonic temperature (T(co)), electrocardiograph (ECG) were monitored during heat exposure (HE) and blood samples were taken 0 and 60 min after HE for IL-1betaassay or nitric oxide (NO) assay. In part 3, additional control and aspirin groups of conscious rats were put in a barrel with 41 degrees C water and kept swimming until drowning over 10 s, and then intervals were recorded as survival time. The results from part 1 showed that from 0 to 50 min after HE, MAPs of control group and aspirin group were not significantly different. About 50-60 min after HE, MAPs of both groups were decreased abruptly and MAPs of control group were decreased significantly in comparison with those of aspirin group. T(co) of both groups was increased until to 42 degrees C, without significant difference. Time of heatstroke onset was not significantly different, while survival time was significantly longer in aspirin group than that in control group. Plasma IL-1betaconcentrations in both groups were significantly increased after HE, and the concentration was significantly higher in the control group than that in aspirin group 60 min after HE. In part 3, the survival time was significantly longer in aspirin group than that in control group. In part 2, MAPs of both groups from 0 to 50 min after HE were not significantly different, whereas 55-60 min after HE, MAPs of control group were decreased significantly in comparison with those of AG group;T(co) of both groups was increased after HE until to 42 degrees C, but without significant difference. The time of the heatstroke onset and survival time of AG group were significantly longer than that of control group;the plasma NO concentrations of two groups were significantly higher 60 min after HE than those 0 min after HE, and the plasma NO concentration of control group was significantly higher than that of AG group 60 min after HE. In conclusion, IL-1betamay contribute to heatstroke through inducing iNOS, which attenuates the tone of peripheral blood vessel, and pretreatment with aspirin can provide preventive effects against heatstroke and reinforce the heat and fatigue endurance, which may be associated with inhibition of systemic IL-1betalevels and local iNOS levels.

[Mechanism of Ca2+ on the hyperthermia-induced apoptosis of rat hippocampal neurons in vitro].

OBJECTIVE: To study the mechanism of Ca(2+) on the apoptosis induced by hyperthermia in neonate rat hippocampal neurons to provide the applicative evidence of dantrolene for preventing brain injuries. METHODS: Dantrolene, Ca(2+) specific blocking agent, was used in the hyperthermia-induced apoptosis of primary hippocampal neurons in vitro to observe its effect on the apoptosis, fluorescent intensity, and dynamic change of Ca(2+) by flowcytometry and laser confocal microscopy. RESULTS: The rate of apoptosis was decreased significantly after hyperthermia treatment by dantrolene sodium. The intracellular Ca(2+) fluorescent intensity in 42 degrees C treatment group (107.35 +/- 6.0) was significantly lower than that in control group (159.12 +/- 33.8). The concentration of Ca(2+) began to decrease 20 approximately 25 s after adding dantrolene sodium, and reached the lowest level about 50 s later, and then kept lower than the basal level. CONCLUSION: Dantrolene sodium has an important protective effect on hippocampal neurons apoptosis induced by hyperthermia and may have some applicative value of preventing heat-induced brain injury.

[Effect of early nutritional support on plasma superoxide dismutase, malondialdehyde and nitric oxide in rats with burns in a hot and humid environment].

OBJECTIVE: To observe the changes of plasma superoxide dismutase (SOD), malondialdehyde (MDA) and nitric oxide (NO) in rats with combined stress of burn injury and hot and humid environment. METHODS: The rats with superficial second-degree scald were subjected to intragastric administration of double-distilled water for one week (control group) or treated with ascorbic acid and L-arginine mixed with a-Tocopherol for one week (treatment group). All the rats were exposed to the same hot and humid environment of Td 37+/-0.5 degrees C with relative humidity of 65%+/-5% for 1-2 h. Observation was performed at 1, 2, 4, and 10 h after the heat exposure, respectively. RESULTS: SOD and MDA changes were significantly different between the two groups (P<0.01, P<0.05). In the control group, NO levels at 1 h were significantly different from those measured at 2 and 6 h after the exposure (P<0.01, P<0.05). CONCLUSION: Early nutritional support can significantly reduce the stress organ injuries, and prevent complications following injury in a hot and humid environment.

[Skin temperature changes in Wistar rats with second-degree scald injury in hot and humid environment after cooling therapy].

OBJECTIVE: To observe the changes in skin temperature after cooling therapy immediate following superficial second-degree scald injury in Wistar rats in a hot and humid environment, and evaluate the effect of the dressing materials for the cooling therapy. METHODS: Twenty-four Wistar rats were randomly divided into normal temperature control (NTC), normal temperature cooling therapy (NCT), hot and humid control (HHC), and hot and humid cooling therapy (HCT) groups (n=6). Different interventions were applied to the scalded rats: dry bulb temperature (Tdb) of 26.33+/-1.29 degree with a relative humidity (rh) of 71.05%+/-4.57% for the two normal temperature groups, and Tdb 35.33+/-0.35 degree with rh of 70.81%+/-1.38% for the two hot and humid environment groups. The dressing materials for the cooling therapy were applied to the two cooling therapy groups but not for the two control groups. The exposure time for the therapy was 125 min, and the skin temperature was measured every 20 min, starting from 5 min after the scald. RESULTS: The skin temperature rose in hot and humid environment and decreased when cold therapy was applied (P<0.001). Interactions were found between the exposure time and environmental temperature (P<0.002), between the exposure time and cooling therapy (P<0.05), and between these 3 factors (P<0.05) to influence the skin temperature, which was 1.92+/-2.13 degrees Celsius lower in NCT group than in NTC group, and 2.36+/-1.03 degrees Celsius lower in HCT group than in HHC group. CONCLUSION: The dressing materials for cooling therapy effectively reduce the skin temperature at the site of the scald injury to prevent the progression of heat-induced injury and the unfavorable effects of the heat remaining on the scalded skin.

[Pretreatment with aspirin for protection against heat stroke in rats].

OBJECTIVE: To observe the changes in blood pressure and interleukin-1beta (IL-1beta) level after heat stroke in rats and to observe the protective effect of pretreatment with aspirin against heat stroke. METHODS: Rat models of heat stroke were established and randomly assigned into control (n=10) and aspirin groups (n=10). Arterial blood pressure, colonic temperature (T(co)), and electrocardiograph (ECG) were monitored and blood samples taken at 0 and 60 min after heat exposure for determining the plasma IL-1beta levels in the two groups. RESULTS: From 0 to 50 min after heat exposure, the mean arterial blood pressure MAP was not significantly different between the two groups, but at about 55-60 min, the MAP significantly decreased in the control group in comparison with the aspirin group (P<0.01). The K value and the height of the dicrotic notch (h(D)/H) were gradually decreased, especially at 40 min after heat exposure, and the control group showed greater reduction in the K value. T(co) of both groups were increased after heat exposure, without significant difference between groups. The time of the onset of heat stroke was similar in the two groups, but rats in the aspirin group had significantly longer survival time (P<0.05). ECG showed that the heart rate and QT intervals of both groups were increased, while PR intervals were decreased after heat exposure. Plasma IL-1beta levels in the two groups were significantly elevated at 60 min in comparison with the basal level (P<0.05), which was more obvious in the control group (P<0.05). CONCLUSION: Pretreatment with anti-inflammatory dose of aspirin can provide protection against heat stroke in rats, which may be associated with the inhibition of elevation of plasma IL-1beta levels by aspirin.

[Protective effects of heat shock response on circulatory collapse induced by hyperthermia].

OBJECTIVE: To investigate the protective effects and mechanism of heat shock response (HSR) on circulatory collapse induced by hyperthermia. METHODS: Two experiments were carried out: (1) Protective effects of HSR. Rats were divided into 2 groups: heat shock (HS) group, sham control (SC) group. After HS group was pretreated with heat shock and recovered for 20 h at room temperature, both groups were exposed to heat till death, and blood pressure, electrocardiogram were measured continuously during exposure. Mean arterial pressure (MAP), survival time etc were acquired through Chart software. (2) Mechanism of effects. Rats were divided into 3 groups: HS group, SC group and normal control (NC) group. The treatment in HS and SC groups was identical with that in the first experiment, but it would be terminated at 73 min after heat exposure. Systolic pressure (Ps), diastolic pressure (Pd) etc were recorded and content of NO and HSP70 in myocardium were measured. RESULTS: (1) The survival time in HS group [(102.3 +/- 11.4) min] was longer than that in SC group [(87.9 +/- 7.7) min] and shock revealed later (P < 0.01); (2) During early heat exposure MAP in HS group was not different from that in SC group, but after 60 min MAP in HS group were higher than that in SC group; (3) MAP, Ps, Pd, HR and HSP70 in HS group were significantly higher but content of NO was lower than those in SC group (P < 0.01, P < 0.05). CONCLUSION: HSR may induce upregulation of HSP70 and inhibit excessive production of NO in myocardium, thus result in relief of circulatory collapse induced by hyperthermia.

[Preventive effects of heat-shock response against circulatory collapse induced by hyperthermia].

OBJECTIVE: To investigate the preventive effects of heat-shock response (HSR) against circulatory collapse induced by hyperthermia and understand its mechanism. METHODS: Twenty-four SD rats were randomized equally into heat-shock group (HS group), high temperature control group (HC group) and normal temperature control group (NC group). The rats in HS group, but not HC group, were subjected to heat shock pretreatment. After a recovery period for 20 h at room temperature, the rats in HS and HC groups were exposed to high temperature environment, and their blood pressures and electrocardiograms were measured continuously. Heat exposure was terminated at 73 min and the contents of myocardial malondialdehyde (MDA) and NO were measured. Using Chart software, the data of the mean arterial pressure (MAP), systolic pressure (SP), diastolic pressure (DP), heart rate (HR) were acquired. The rats in NC group did not receive any treatment to obtain the measurements in normal condition. RESULTS: Compared with NC group, the MAP, SP and DP were significantly lowered (P P<0.01) in HS and HC group and HR accelerated (P P<0.01) after a 73-min heat exposure, and HS group had significantly higher measurements of the above indices than HC group did. In comparison with NC group, the contents of MDA and NO in the myocardium in HC group were significantly elevated after the exposure (P P<0.01). The MDA content in HS group, which was comparable with that of NC group, was significantly lower than that of HC group (P P<0.05), and compared with HC group, HS also had lower NO content (P<0.01). CONCLUSION: HSR may relieve circulatory collapse induced by hyperthermia, which involves the inhibitory effect of HSR on the production of MDA and NO in the myocardium.

[Effect of cooling therapy on the heart rate and mean arterial pressure of rats with the second-degree scald burn in hot and humid environment].

OBJECTIVE: To observe the changes of heart rate (HR) and mean arterial pressure MAP after immediate cooling therapy (ICT) in rats with superficial second-degree scald burn in hot and humid environment, and assess the effect of the cooling dressing materials. METHODS: Twenty-four Wistar rats were randomized equally into 4 groups including normal temperature control (NTC) group, normal temperature cooling therapy (NCT) group, hot and humid control (HHC) group and hot and humid cooling therapy (HCT) group. Different interventions were applied as indicated in the rats with superficial second-degree scald burn, with the dry bulb temperature Tdb at 26.33+/-1.29 degrees celsius; and relative humidity (rh) of 71.05%+/-4.57% for two normal temperature groups, and Tdb at 35.33+/-0.35 degrees Celsius; and rh of 70.81%+/-1.38% for the two hot and humid groups. The exposure time was 120 min in NCT and HCT groups, and the HR and MAP were measured every 20 min. RESULTS: MAP is not influenced by environmental temperature and the cooling therapy (P>0.05), whereas HR was higher in HHC than in NTC group and also in HCT than in NCT group (P=0.003), lower in HCT and NCT groups than in HHC and NTC groups (P=0.002), respectively. HR did not undergo any significant changes during the observation in the 4 groups (P>0.05). HR was higher in HHC and HCT than in NTC and NCT groups at 65, 85, 105 and 125 min after the burns, but compared with the two control groups, cooling therapy decreased HR at 5, 25, 45 and 85 min. CONCLUSION: Cooling therapy does not affect MAP but efficiently decreases HR, which may prevent further heat injury.

Rectal temperature changes of Wistar rats with second-degree scald burn in hot and humid environment following immediate cooling therapy.

OBJECTIVE: To observe the changes in rectal temperature (Tr) after immediate cooling therapy for Wistar rats with superficial second-degree scald burn in hot and humid environment, and evaluate the effect of the dressing material for cooling. METHODS: Twenty-four Wistar rats were randomly divided into 4 groups (n=6), namely normal temperature control (NTC), normal temperature cooling therapy (NTCT), hot and humid control (HHC), and hot and humid cooling therapy (HHCT) groups. Superficial second-degree scald burns were induced in the rats, followed by interventions with cooling therapy in the two therapy groups at dry bulb temperature (Tdb) of 35.33+/-0.35 degrees Celsius with relative humidity of 70.81%+/-1.38%, whereas the two control groups were treated at Tdb of 26.33+/-1.29 degrees Celsius with relative humidity of 71.05%+/-4.57% without dressing for cooling therapy. The exposure time of each group was 120 min, and the Tr was recorded every 20 min. RESULTS: On the basis of comparisons between the measurements taken at 7 different time points, we found that the Tr of the rats was elevated in hot and humid environment (P<0.001) and decreased when cooling therapy was applied (P<0.001). Interactions between the environmental temperature and cooling therapy were noted in their influence on Tr (P=0.003). As the exposure time was prolonged, Tr slowly decreased in NTC group, mildly fluctuated in NTCT group, but elevated in HHC and HHCT groups with gradual increase of the differences between the measurements taken at the same time point. CONCLUSION: Application of the dressing material on the abdomen for cooling therapy can efficiently lower the Tr, which may prevent the progression of the heat injury.

[Effects of combined stress on rabbit serum and gastroduodenal mucosa motilin and its mechanism].

OBJECTIVE: To study the effects of heat exposure and trauma stress on the level of motilin (MTL) in plasma and the distribution of MTL gastroduodenal mucosa and its mechanism in rabbits. METHODS: The rabbits were randomly divided into four groups, control group, trauma group (23 centigrade degree), heat exposure group (38 centigrade degree) and heat exposure combined trauma group. The MTL was measured by radioimmunoassay (RIA). The rabbit model of heat exposure with trauma was established. The levels of the MTL were measured at 0, 0.5, 1, 1.5 and 2 hours during experiment. RESULTS: In control group, the concentration of MTL was highest in gastric corpus, and then were gastric fundus, pylorus and Duodenal mucous membrane. The concentration of MTL was higher in plasma than that in tissues. After heat exposure and trauma, the concentration of MTL decreased in tissues and increased in plasma. CONCLUSION: The concentration of MTL was different in different parts of gastroduodenal mucosa. The heat exposure and trauma stress may result in the converse changes of the level of MTL in plasma and tissues. The mechanism might be that the destroyed Mo cells released MTL and increasing level of bombesin stimulated by stress induced the release of MTL.