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AbstractUncovering the collective behavior of flows among locations is critical to understanding the structure within an ever-changing spatial network. When a network evolves, there may exist subgraphs within which the internal flows generally follow a rule: the change rates of the flow weight are either collectively high or low. Classic network measures such as degree, clustering, and betweenness can be used to quantify the process of network evolution by profiling the overall characteristics over time. However, it remains challenging to elucidate how a spatial network is evolving without looking at structures where collective changes emerge. To bridge this gap, we introduce the concept of the Collective Flow-Evolutionary Pattern (CFEP) as a mesoscopic description for spatial network evolution. Four types of patterns with distinct features are defined to clarify the collective behaviors of the flow-evolutionary characteristics. We provide an analytical framework that utilizes flow change rates between two snapshots of the spatial network to detect CFEPs as optimized flow evolution (evo-groups). Synthetic experiments are presented to validate the method. A case study of large-scale individual mobile positioning data is conducted in the Twin Cities Metropolitan Area, Minnesota, US to demonstrate how CFEP can effectively understand the evolution of human mobility networks. [ABSTRACT FROM AUTHOR]

Given the complex characteristics of city structure, the analysis of tourists' activities in urban space is challenging. Previous studies on urban tourists' activities were mostly limited to official administrative units, such as attractions, blocks, and administrative districts, and rarely considered the multi-scale characteristics of urban tourism space. This study offered insights into urban tourism by depicting multi-scale tourism spaces from the perspective of tourists' activities. Based on a spatial conceptual model, the urban destination was divided into multi-scale spaces, including tourist areas of interest (areas of intensive tourist activity), attraction-community complexes (comprising tourist attractions and supporting service facilities), and tourism districts (subregions with different tourism types). The Geographic Information System field and spatial interaction models were combined to identify multi-scale tourist activity spaces using digital footprints from geolocated social media data. The proposed framework was verified in Suzhou, a typical urban destination in China, which confirmed that the systematic and comprehensive methodology could be used as a tool for smart urban destination management and planning based on tourists' demands. [ABSTRACT FROM AUTHOR]

Purpose Many patients suffer from chronic postsurgical pain (CPSP) following surgery, and the underlying mechanisms are poorly understood. In the present work, using the skin/muscle incision retraction (SMIR) model, the role of spinal TLR4/TNF-[alpha] pathway in the induction of CPSP was evaluated. Methods Mechanical allodynia induced by SMIR was established in adult male Sprague-Dawley rats. The von Frey test was performed to evaluate the role of TLR4/TNF-[alpha] pathway on the mechanical allodynia. Western-blot and immunohistochemistry methods were adopted to understand the molecular mechanisms. Results SMIR surgery decreased the ipsilateral 50 % paw withdrawal threshold, lasting for at least 20 days. Western-blot analysis and immunohistochemistry revealed that SMIR surgery significantly upregulated the expression of TLR4 (p < 0.01) in glial cells on the ipsilateral side of spinal cord and increased TLR4 occurred on day 5 and was maintained to the end of the experiment (day 20). Similarly, tumor necrosis factor-alpha (TNF-[alpha]) was significantly increased on days 5, 10, and 20 on the ipsilateral side of spinal dorsal horn following SMIR surgery. Intraperitoneal injection of an inhibitor of TNF-[alpha] synthesis thalidomide at 50 or 100 mg/kg dose (but not 10 mg/kg dose) significantly ameliorated the reduced paw withdrawal threshold induced by SMIR surgery. Importantly, intrathecal delivery of a specific TLR4 antagonist (LPS-RS) at dose of 25 [mu]g significantly attenuated mechanical allodynia and prevented the upregulation of TNF-[alpha] induced by SMIR surgery. Conclusions These findings suggest that the upregulation of TNF-[alpha] via TLR4 contributes to the development of CPSP in spinal dorsal horn., Author(s): Yang Sun[sup.2] , Mingmin Yang[sup.2] , Hao Tang[sup.1] , Zhongfu Ma[sup.1] , Yanbing Liang[sup.1] , Zhenyu Li[sup.1] Author Affiliations: (1) Department of General Internal Medicine, The First Affiliated Hospital [...]

Exposure to particulate matter ≤2.5 µm in diameter (PM2.5) profoundly affects human health. However, the role of PM2.5 on lung injury and cytokine levels in mice is currently unknown. The aim was to examine the effect of PM2.5 pollution on lung injury in mice fed at an underground parking lot. A total of 20 female Kunming mice were randomly divided into control and polluted groups, with 10 rats in each group. The control group was kept in the laboratory, while the pollution group was fed in an underground parking lot. The concentrations of pollutants were measured using ambient air quality monitoring instruments. After 3 months of treatment, the lungs were collected and examined using electron microscopy, and the morphological structures were assessed using hematoxylin and eosin staining. The polarization of macrophages was evaluated by immunofluorescence. The concentration of interleukin (IL)-4, tumor necrosis factor (TNF)-α and transforming growth factor (TGF)-β1 in peripheral sera were assessed by ELISA. The mRNA and protein levels of IL-4, TNF-α, and TGF-β1 in lung tissues were assessed by reverse transcription-quantitative polymerase chain reaction and western blot analyses, respectively. In the polluted group, the levels of CO, NOx and PM2.5 were significantly higher compared with the control group. Compared with the controls, intracellular edema, an increased number of microvilli and lamellar bodies, smaller lamellar bodies in type II alveolar epithelial cells, and abundant particles induced by PM2.5 in macrophages were observed in the polluted group. The lung ultrastructure changed in the polluted group, revealing exhaust-induced lung injury: The tissues were damaged, and the number of inflammatory cells, neutrophils, polylymphocytes and eosinophils increased in the polluted group compared with the control group. The authors also observed that the number of M1 and M2 macrophages markedly increased after the exhaust treatment. The levels of IL-4, TNF-α and TGF-β1 in the sera and tissues were significantly increased in the polluted group. PM2.5 pollutants in underground garages can lead to lung injury and have a significant impact on the level of inflammatory cytokines in mice. Therefore, the authors suggest that PM2.5 can activate the inflammatory reaction and induce immune dysfunction, leading to ultrastructural damage. [ABSTRACT FROM AUTHOR]

Anastrozole is currently used as first‐line treatment in locally advanced or metastatic breast cancer. A generic anastrozole tablet was developed to offer an alternative to the marketed tablet formulation. The aim of the current study was to evaluate the bioequivalence between the test and reference formulations of anastrozole in a single‐dose, 2‐period, 2‐sequence crossover study with a 14‐day washout interval. A total of 20 healthy male Chinese volunteers were enrolled and completed the study, after oral administration of a single dose of 1.0‐mg test and reference formulations of anastrozole. The blood samples were collected at different times and were determined by a fully validated high‐pressure liquid chromatography–tandem mass spectrometry method. The evaluated pharmacokinetic parameters, including Cmax, AUC0–t, and AUC0–∞, were assessed for bioequivalence based on current guidelines. The observed pharmacokinetic parameters of anastrozole of the test drug were similar to those of the reference formulation. The 90% confidence intervals of test/reference ratios for Cmax, AUC0−t, and AUC0−∞ were within the bioequivalence acceptance range of 80%–125%. The results obtained from these healthy Chinese subjects in this study suggest that the test formulation of anastrozole 1.0‐mg tablet is bioequivalent to the reference formulation (Arimidex 1.0‐mg tablet). [ABSTRACT FROM AUTHOR]

Exposure to particulate matter ≤2.5 µm in diameter (PM 2.5 ) profoundly affects human health. However, the role of PM 2.5 on lung injury and cytokine levels in mice is currently unknown. The aim was to examine the effect of PM 2.5 pollution on lung injury in mice fed at an underground parking lot. A total of 20 female Kunming mice were randomly divided into control and polluted groups, with 10 rats in each group. The control group was kept in the laboratory, while the pollution group was fed in an underground parking lot. The concentrations of pollutants were measured using ambient air quality monitoring instruments. After 3 months of treatment, the lungs were collected and examined using electron microscopy, and the morphological structures were assessed using hematoxylin and eosin staining. The polarization of macrophages was evaluated by immunofluorescence. The concentration of interleukin (IL)-4, tumor necrosis factor (TNF)-α and transforming growth factor (TGF)-β1 in peripheral sera were assessed by ELISA. The mRNA and protein levels of IL-4, TNF-α, and TGF-β1 in lung tissues were assessed by reverse transcription-quantitative polymerase chain reaction and western blot analyses, respectively. In the polluted group, the levels of CO, NO x and PM 2.5 were significantly higher compared with the control group. Compared with the controls, intracellular edema, an increased number of microvilli and lamellar bodies, smaller lamellar bodies in type II alveolar epithelial cells, and abundant particles induced by PM 2.5 in macrophages were observed in the polluted group. The lung ultrastructure changed in the polluted group, revealing exhaust-induced lung injury: The tissues were damaged, and the number of inflammatory cells, neutrophils, polylymphocytes and eosinophils increased in the polluted group compared with the control group. The authors also observed that the number of M1 and M2 macrophages markedly increased after the exhaust treatment. The levels of IL-4, TNF-α and TGF-β1 in the sera and tissues were significantly increased in the polluted group. PM 2.5 pollutants in underground garages can lead to lung injury and have a significant impact on the level of inflammatory cytokines in mice. Therefore, the authors suggest that PM 2.5 can activate the inflammatory reaction and induce immune dysfunction, leading to ultrastructural damage., (Copyright: © Yang et al.)

This study was performed to evaluate the cardioprotective effects of osthole (OST) in a rat model of myocardial ischemia/reperfusion injury (MI/RI) and the underlying mechanism. We exposed rat hearts to left anterior descending coronary artery ligation for 30 min followed by 24 h of reperfusion. The results showed that pretreatment with OST ameliorated MI/RI as evidenced by histopathological examination. Moreover, the terminal deoxynucleotidyl transferase dUTP nick end-labeling assay demonstrated that OST suppressed myocardial apoptosis, which may be related to an increase in the Bcl-2/Bax ratio and inhibition of caspase-3 and caspase-9 activation. Furthermore, we determined that OST ameliorated impaired mitochondrial morphology and the oxidation system; OST also attenuated levels of pro-inflammatory cytokines, including tumor necrosis factor α and interleukins 6 and 1β. In conclusion, OST exerted a strong favorable cardioprotective effect on MI/RI, possibly by suppressing the inflammatory response and inhibiting cell apoptosis., Competing Interests: None.

Rhein is an important component in traditional Chinese herbal medicine formulations for gastrointestinal disorders, including inflammatory bowel diseases such as ulcerative colitis. In this study, we investigated the beneficial effects of rhein in inflammation models in the transgenic zebrafish line TG (corolla eGFP), in which both macrophages and neutrophils express eGFP and RAW264.7 macrophages. We found that the tail-cutting-induced migration of immune cells was significantly reduced in transgenic zebrafish treated with rhein. In addition, the production of proinflammatory cytokines, including IL-6, IL-1β, and tumor necrosis factor-α, were significantly reduced in lipopolysaccharide (LPS)-induced RAW264.7 macrophages treated with rhein. Parallel to the inhibition of proinflammatory cytokines, rhein significantly reduced phosphorylation levels of NF-κB p65 and inducible nitric oxide synthase, as well as COX-2 protein expression levels. Furthermore, rhein significantly reduced NALP3 and cleaved IL-1β expression in LPS + ATP-induced RAW264.7 macrophages. Thus, the present study demonstrates that rhein may exhibit its anti-inflammatory action via inhibition of NF-κB and NALP3 inflammasome pathways., Competing Interests: Disclosure The authors report no conflicts of interest in this work.

Objective: To observe the protective effects of recombinant trichinella spiralis-53 000 protein (rTsP53 protein) combining with imipenem (IMP) on septic mice and their underlying mechanisms. ., Methods: Male BALB/c mice were divided into five groups randomly. Cecal ligature and puncture (CLP) operation was used for building polymicrobial septic model (CLP group).Mice in sham group were only subjected to laparoromy and abdominal closure without cecum ligation. At 6 hours post CLP, mice in CLP+IMP,CLP+rTsP53,and CLP+IMP+rTsP53 groups were injected intraperitoneally with IMP (20 mg/kg) + 0.1 mL albumin,rTsP53 protein (6 mg/kg) + 0.1 mL normal saline (NS),IMP (20 mg/kg) + rTsP53 protein (6 mg/kg) respectively, mice in sham group and CLP group were injected intraperitoneally with 0.1 mL albumin + 0.1 mL NS, then these therapies were repeated every 12 hours until the experiment ended. Twenty mice were extracted randomly from each group for surveying 72-hour survival rate.At 0,6,12,24,36,48,72 hours post CLP,3 mice in each group were collected and cytokines in serum were tested by enzyme-linked immunosorbent assay (ELISA).Whole blood was cultured, then the numbers of bacteria colony-forming units (CFU) were counted. Mice were executed at 24 hours, then the epithelial cells ultrastructures of the mice small intestinal mucosa were observed by transmission electron microscope (TEM)., Results: ① Compared with CLP,CLP+IMP or CLP+rTsP53 group,72-hour survival rate of the mice in CLP+IMP+rTsP53 group was significantly elevated (85％ vs.20％,55％,25％,all P ＜ 0.05).② No bacteria was found in cultured whole blood of mice in sham group at all time-points. At 6 hours post CLP operation, the number of bacterial clone of all experimental groups was rose significantly. The changed trend of bacterial number in CLP group was rising at the beginning, then declining, and the bacterial number reached the peak at 24 hours (× 106 cfu/L:12.74± 2.33).From 12 hours, the bacterial numbers of CLP+rTsP53 group were higher than those of CLP group, and reached the peak at 36 hours (× 106 cfu/L:22.13 ± 4.28),then declined gradually. The bacterial numbers of CLP+IMP and CLP+IMP+rTsP53 groups reached the peak at 6 hours (× 106 cfu/L:5.72 ± 0.50,5.49 ± 0.59),then declined. They were significantly less than those of CLP group from 12 hours.③ From 6 hours after CLP,the cytokines levels of mice in all experimental groups were higher than those in sham group. The tumor necrosis factor-α (TNF-α) levels in CLP group showed a trend of elevation in the beginning, and decrease thereafter. It reached the peak at 36 hours (ng/L:1 422.67 ±72.19).The TNF-α level peak time of CLP+IMP group,CLP+rTsP53 group,CLP+IMP+rTsP53 group was advanced to 12 hours post CLP (ng/L:1376.29±44.67,929.36±40.42,809.61±22.61).At 24 hours post CLP, the interleukin-6 (IL-6) level of CLP group and CLP+IMP group reached the peak (ng/L:215.39 ± 16.05,191.63 ± 8.99).The peak time of CLP+rTsP53 group and CLP+IMP+rTsP53 was advanced to 12 hours post CLP (ng/L:113.01 ± 12.11,92.43±6.11).The level of IL-4,IL-10 in CLP group raised gradually to the highest at 72 hours (ng/L:366.25 ±24.25,923.14±30.36).The IL-4 and IL-10 levels of CLP+IMP group raised to their maximum value at 12 hours and 24 hours respectively (ng/L:281.47±16.33,555.67±13.57),then declined. The IL-4 and IL-10 levels of CLP+rTsP53 group and CLP+IMP+rTsP53 group gradually ascended their peak value at 72 hours [IL-4 (ng/L) was 453.14±18.53,410.43 ± 15.75,IL-10 (ng/L) was 1 185.61 ± 16.74,1 006.77 ± 36.91,respectively].From 12 hours, the pro-inflammatory cytokines levels of CLP+IMP+rTsP53 group were significantly less than those of CLP+IMP group and CLP+rTsP53 group.④ At 24 hours post CLP, compared with mice in CLP,CLP+IMP, or CLP+rTsP53 group, mice in CLP+IMP+rTsP53 group had slighter ultra structure injuries in the microvilli, cell junction and mitochondria of small intestinal mucosa epithelial cells., Conclusions: The levels of pro-inflammatory cytokines were reduced and the levels of anti-inflammatory eytokines were escalated by intervention of rTsP53 protein combining with IMP boosted in polymierobial septic mice serum, and enhanced the survival rate of the mice. The injection of rTsP53 protein alone had no protective effects on polymicrobial septic mice,because the amount of bacteria in mice blood was augmented

Objective: To investigate the value of serum cholinesterase (S-ChE) levels in judgment of severity and prognosis in patients with severe pneumonia., Methods: The clinical data of patients with severe pneumonia, who were admitted to the Department of Internal Medicine in the First Affiliated Hospital of Sun Yat-sen University, or the Department of Neurology in the Third People's Hospital of Foshan from May 2011 to May 2015, whose hospital time was longer than 24 hours, were retrospectively analyzed. They were divided into survival group and death group according to the final outcome. Lab data, acute physiology and chronic health evaluation II (APACHE II) score, multiple organ dysfunction syndrome (MODS) score, the improved pneumonia score of British Thoracic Society (confusion, uremia, respiratory, blood pressure, age 65 years, CURB-65), and S-ChE levels of all patients were collected after they were hospitalized into the intensive care unit (ICU) within 24 hours. Independent risk factors for prognosis were analyzed by binary logistic regression analysis, and receiver operating characteristic curve (ROC) was plotted. Best truncation point analysis was used to compare their estimated value for prognosis of patients with severe pneumonia., Results: Eighty-six patients with severe pneumonia were studied. Among them 46 patients survived, and 40 patients died. By the single factor analysis, the following lab data in the death group were found significantly lower than those in the survival group: S-ChE levels (kU/L: 2.748±0.826 vs. 4.489±1.360, t' = 7.274, P = 0.000), arterial partial pressure of oxygen [PaO2 (mmHg, 1 mmHg = 0.133 kPa): 52.55±18.29 vs. 60.83±16.65, t = 2.196, P = 0.031], oxygenation index (mmHg: 114.20±48.01 vs. 167.10±69.68, t' = 4.229, P = 0.000), and carbon dioxide combining power [CO2-CP (mmol/L): 22.85±5.44 vs. 26.00±7.63, t' = 2.225, P = 0.029]. The following clinical data were significantly higher in the death group than those in the survival group, namely body temperature (centigrade: 38.67±1.18 vs. 37.74±1.18, t = -3.627, P = 0.000), pulse (bpm: 130.65±15.72 vs. 107.26±19.61, t' = -6.133, P = 0.000), the ratio of concomitant chronic lung disease [45.0% (18/40) vs. 13.0% (6/46), χ(2) = 10.860, P = 0.001], fraction of inspired oxygen [FiO2: 0.495 (0.410, 0.600) vs. 0.380 (0.290, 0.500), Z = -3.265, P = 0.001], APACHE II score (25.80±5.07 vs. 16.39±5.12, t =-8.540, P = 0.000), CURB-65 score [3 (3, 4) vs. 2 (1, 2), Z = -5.562, P = 0.000], MODS score (8.15±2.49 vs. 4.35±2.01, t = -7.832, P = 0.000), international normalized ratio [INR: 1.22 (1.08, 1.31) vs. 1.07 (1.00, 1.10), Z = -4.231, P = 0.000], and activated partial thromboplastin time [APTT (s): 33.80 (32.13, 38.75) vs. 28.50 (25.70, 36.00), Z = -3.482, P = 0.000]. Binary logistic regression analysis showed that, S-ChE levels, APACHE II score and MODS score were found to be the independent risk factors for prognosis in the patients with severe pneumonia, respectively [S-ChE: odds ratio (OR) = 0.084, 95% confidence interval (95%CI) = 0.017-0.424, P = 0.003; APACHE II score: OR = 1.675, 95%CI = 1.098-2.556, P = 0.017; MODS score: OR = 2.189, 95%CI = 1.262-3.800, P = 0.005]. The area under ROC (AUC) for S-ChE levels, APACHE II score and MODS score were 0.874±0.036, 0.889±0.033 and 0.884±0.035, respectively (all P > 0.05 as compared between any two means). At the best truncation points of S-ChE levels, APACHE II score and MODS score were 3.372 kU/L, 19.5 score, and 6.5 score respectively. The sensitivity, specificity, positive predictive value and negative predictive value in predicting death risk in patients with severe pneumonia were (80.0%, 78.0%, 76.19% and 81.82%), (95.0%, 70.0%, 73.08% and 94.12%) and (70.0%, 91.0%, 87.50%, 77.78%), respectively. If S-ChE levels was combined with APACHE II score or combined with MODS score, the sensitivity, specificity, positive predictive value and negative predictive value [S-ChE levels combined APACHE II score: 100%, 92.0%, 93.75% and 100%; S-ChE levels combined MODS score: all 100%] were higher than single power of S-ChE levels, APACHE II score or MODS score., Conclusions: S-ChE levels can be considered as an effective and practical index to estimate the severity and prognosis in patients with severe pneumonia. The combined application of S-ChE levels and APACHE II score or MODS score can obviously improve the prognostic power in patients with severe pneumonia.

We investigated that if rTsP53 could be used to activate bone-marrow derived macrophage (BMDM) into M2 macrophage and stop M1 macrophage activation. After 72 h incubation in blank culture medium, cells with PE-CCR7 (-) and FITC-CD206 (-) was extracted and its mean proportion was 92.30 ± 0.22%. With the stimulation of 20 μg/ml IFN-γ for 72 h, cells with PE-CCR7 (+) was extracted and its mean proportion was 16.24 ± 0.82%. With the stimulation of IL-3/IL-14 (both 10 μg/ml) for 72 h, cells with FICT-CD206 (+) was extracted and its mean proportion was 87.32 ± 4.29%. Co-incubation with different dose of rTsP53 (0.001 μg/ml, 0.01 μg/ml, 0.1 μg/ml, 1 μg/ml, 2 μg/ml, 5 μg/ml, 10 μg/ml, respectively) for 72 h, FITC-CD206 (+) macrophage was extracted. The mean proportion in each group was 1.09 ± 0.22%, 2.13 ± 0.13%, 4.91 ± 0.07%, 5.48 ± 0.29%, 9.81 ± 0.06%, 12.83 ± 0.55%, 17.87 ± 0.02%, respectively. The dose of rTsP53 was significantly positive correlated to the proportion of FITC-CD206 (+) macrophage. Co-incubation with 20 μg/ml IFN-γ and 5 μg/ml rTsP53 for 72 h, cells with PE-CCR7 (+) was extracted and its mean proportion was 10.60 ± 0.19%. Compared to that of mere co-incubation with IFN-γ, there was significant difference between the two groups. ELISA showed that Th1 cytokines' (IFN-γ, IL-6 and TNF-α) level decreased in the culture medium supernatant of BMDM co-incubated with rTsP53. There was negative correlation between the Th1 cytokines' level and the dose of rTsP53. Both Th2 cytokines (IL-4 and IL-13) and regulatory cytokines in the culture medium increased. There was positive correlation between the Th2 cytokines' level and the dose of rTsP53. There was also positive correlation between the regulatory cytokines' level and the dose of rTsP53. Compared to that of BMDM co-incubated with IFN-γ, levels of TNF-α and IL-6 were significant lower than that of BMDM co-incubated with both IFN-γ and rTsP53 (both P < 0.05), while the levels of IL-4 and TGF-β were significant higher (both P < 0.05). There was no significant difference in the levels of IL-13 and IL-10 between the two groups.

Objective: To evaluate if recombinant Trichinella spiralis-53 000 protein (rTsP53) could alleviate liver damage caused by lipopolysaccharides (LPS) via M2 macrophage activation., Methods: Sixty male BALB/c mice were randomly divided into LPS group, LPS + phosphate buffer saline (PBS) group and rTsP53 intervention group by random number table, with 20 mice in each group. Intraperitoneal injection of 15 μg/kg LPS was performed for all the mice in the three groups after 8 hours of fasting. The mice in LPS + PBS group were injected with PBS after 1 hour of LPS injection. The mice in the rTsP53 intervention group were injected with rTsP53 (5 mg/kg) after 1 hour of LPS injection. After 48 hours all the mice were sacrificed. Peritoneal macrophages were harvested and flow cytometry (FCM) was used to detect markers CCR7 (M1) and CD206 (M2) of macrophages. Hepatic tissue was harvested for pathological study after hematoxylin-eosin (HE) staining, and double staining immunofluorescence was used to detect F4/80⁺ HLA-DR⁺ and F4/80⁺ CD163⁺. Peripheral blood serum was harvested to detect the levels of aspartate transaminase (AST) and alanine transaminase (ALT)., Results: Compared with LPS and LPS + PBS groups, survival rate of mice of rTsP53 intervention group was significantly elevated (90% vs. 25%, 30%, both P<0.01), and the pathological injury of the liver was significantly ameliorated, and the hepatic structure was better preserved. The transaminase in rTsP53 intervention group was significantly lower than that of LPS and LPS + PBS groups (ALT: 97.7 ± 8.5 U/L vs. 181.7 ± 19.5 U/L, 173.7 ± 17.2 U/L; AST: 142.7 ± 12.1 U/L vs. 235.7 ± 9.9 U/L, 213.7 ± 6.7 U/L, all P<0.05), FITC-CD206⁺ proportion of peritoneal macrophage was significantly higher [(17.75 ± 0.30)% vs. (1.38 ± 0.13)%, (1.36 ± 0.05)%, both P<0.05] while PE-CCR7(+) proportion [(6.89 ± 0.11)% vs. (15.30 ± 0.64)%, (14.96 ± 0.93)%, both P<0.05] was significantly lower. Fluorescence intensity of macrophages with F4/80⁺ CD163⁺ double staining for liver sections was significantly increased (0.36 ± 0.01 vs. 0.29 ± 0.02, 0.31 ± 0.01, both P<0.05), while there was no significant difference in the fluorescence intensity of macrophages with F4/80⁺ HLA-DR⁺ double staining (0.30 ± 0.01 vs. 0.30 ± 0.02, 0.31 ±0.01, both P>0.05). There was no significant difference of above results between LPS group and LPS + PBS group (all P>0.05)., Conclusions: rTsP53 could ameliorate liver damage caused by LPS and improve animal's survival via the activation of M2 macrophage.