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Objective To investigate the effect of the monocytes/macrophages on acute lung injury in rats with severe heatstroke, by modulating the expression of triggering receptor expressed on myeloid cells-1 (TREM-1). Methods Forty rats were randomized evenly into the control group (Con group), heatstroke group (HS group), the low dose inhibitor group (LD group) and the high dose inhibitor group (HD group). Before heatstroke induction, the rats of LD and HD groups were administrated with a 50 mg/kg and 100 mg/kg bolus of LP-17, respectively. All rats were exposed to an environment with temperature of (40±2) ℃ and humidity of 65%±5% for 60 minutes to induce heatstroke. Enzyme-linked immunosorbent assay (ELISA) was utilized to quantify the concentration of tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and IL-1β in the peripheral blood and pulmonary tissue. The expression of TREM-1 on peripheral monocytes was identified by flow cytometry. Moreover, the histological phenotypes were evaluated after HE stain and the expression of inducible nitric oxide synthase (iNOS) was analyzed by immunohistochemistry in pulmonary tissues. Furthermore, Western blotting was used to detect the protein level of TREM-1 and monocyte chemoattractant protein-1 (MCP-1). Results Compared to HS rat, in rats pretreated with LP-17, the levels of TNF-α, IL-6 and IL-1β in peripheral blood (P

Objective To investigate the plasma exosome S100P levels in patients with heatstroke and evaluate its clinical diagnostic value. Methods Thirty heatstroke patients were selected from June 2016 to June 2018 in the General Hospital of Southern Theatre Command of PLA, and 15 healthy people in the Physical Examination Center of our hospital were selected as control. The venous blood was collected, followed by plasma exosomes extraction using polyethylene glycol precipitation. The plasma exosome S100P was quantified by ELISA. The correlation analysis between plasma exosomal S100P, clinical indicators, and disease severity was performed. The receiver operating characteristic (ROC) curve was analyzed to evaluate the efficacy of plasma exosome S100P in diagnosing heatstroke. Results The level of plasma exosomes S100P in patients with heatstroke significantly increased [healthy people vs. heatstroke patients: (195.89±131.97) pg/ml vs. (1163.62±747.15) pg/ml, P

Objective To study the change of the contractile response of human umbilical artery smooth muscle cells (HUASMCs) during the heat stress, and explore the effect of the antioxidant on the changes. Methods HUASMCs were randomly divided into control group, heat stress group, antioxidant preprocessing group. Cells were stimulated by norepinephrine (NE) at a low concentration (0.05mg/L) and at a normal concentration (1.0mg/L) and cultured in the thermostatic water bath (41℃) for 0.5, 1, 1.5 or 2h, respectively. After stimulated by NE, proportion of the cell surface area contraction was measured to reflect the contractile response of each group. Results Compared with control group, regardless of the NE concentration: in heat stress group, contractile response at 1h increased significantly (P0.05), but in the antioxidant preprocessing group, the contractile response was more significant to the normal NE concentration than to the low NE concentration (P

Objective To investigate the effect of gradient heat stress on phagocytosis of hepatic Kupffer cells (KCs) in vitro in rats. Methods Rat Kupffer cells were isolated in vitro and the temperature for gradient heat stress was set at 37, 39, 41 and 43℃. After thermal stimulation, cell injury was detected by PI and Hochest33342 staining. CCK-8 assay was used to investigate difference in cellular proliferation rate over 24h between the groups. Flow cytometry was used to investigate the influence of heat stress on the phagocytosis of KCs. Results Compared to the normal control group, cells in each heat stress group exhibited varying degrees of damage, especially cells in 43℃ group. The ratio of damage cells increased with the increase of heat stress severity (P

Objective To examine the effects of ulinastatin (UTI) on cardiac dysfunction in mice with heat stroke and its possible mechanism. Methods 20 mice were divided into four groups randomly: room temperature plus normal saline (Sham+NS), room temperature plus UTI (Sham+UTI), heat stress plus normal saline (HS+NS), heat stress plus UTI (HS+UTI), 5 each. 105U/kg UTI was delivered by intraperitoneal injection before the onset of the heat stress. Room temperature groups were housed at room temperature (23.0±0.5℃), while heat stress groups were kept in an incubator at 36.5±0.5℃ and humidity of 65.0%±2.0%. The rectal temperature (Tr) reaching 42℃ was taken as severe heat stroke, and the time in two heat stress groups was recorded. The mice were transferred to the room temperature (23.0±0.5℃) for natural cooling after the heat stroke onset. 6 hours after the treatment, cardiac output (CO) was ultrasonographically detected, the myocardium was separated for histopathological examination and the expression of total p38 and phosphorylated p38 (p-p38) was determined by Western blotting. Results The time to reach 42℃ in HS+UTI group was significantly prolonged (P=0.044). Compared with the Sham+NS group, the CO in HS+NS and HS+UTI group decreased significantly (P=0.017), and the score of myocardial inflammation (P

Objective To investigate the heat stress-induced dysfunction of intestinal barrier including intestinal tight junction and apoptosis of epithelial cells. Methods Human intestinal epithelial Caco-2 cell monolayers, serving as the intestinal barrier model, were exposed to different temperature (37-43℃) for designated time. Transepithelial electrical resistance (TEER) and horseradish peroxidase (HRP) flux permeability were measured to evaluate barrier integrity. Level of tight junction (TJ) protein occludin was analyzed by Western blotting. Cell apoptosis rate was determined using Annexin V-FITC/PI kit by flow cytometry. Results Compared with the 37℃ group, TEER lowered and the permeability for HRP increased significantly after heat exposure (P