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Increasing attention is being paid to hydrothermal carbonization (HTC) of waste biomass, due to energy shortages, environmental crises and developing customer demands. However, most research has been dedicated to the production of bio-oil, with few studies focusing on the application of hydrothermal carbon (hydrochar), a solid residue from HTC of biomass. In this study, a novel porous carbon (PC) was prepared from hydrochar, via pyrolysis at different temperatures (300-700°C), the characteristics of PC as well as tetracycline (TC) adsorption behavior were investigated. The hydrochar and PC samples showed a remarkable range of surface properties, as characterized by Boehm titration, the Fourier transform infrared spectra and nuclear magnetic resonance spectra. The changes in characteristics suggested that the PC samples produced at high activation temperature (500-700°C) were well carbonized and exhibited a high surface area (>270m²/g). Linear relationships were obtained between Freundlich adsorptive capacity (KF) and elemental atomic ratios, surface area and pore volume. The high adsorption capacity of PC samples can be attributed to its low polarity and high aromaticity, surface area and pore volume. The molecular variations among the hydrochar and PC samples translated into differences in their ability to adsorb TC. [ABSTRACT FROM AUTHOR]

Bio-oil obtained from hydrothermal liquefaction of Salix psammophila is a very complicated mixture with some highly valued chemicals. In order to separate the chemicals from bio-oil, solvent extraction using nine solvents with different polarities were investigated in detail. The bio-oil extraction yield of the nine solvents were from high to low: tetrahydrofuran > toluene > ethyl acetate > acetone > ether > methylene chloride > methanol > petroleum ether > n-hexane. Based on their extraction yield, an efficient solvent combination of n-hexane, ethyl acetate, and tetrahydrofuran was used to separate the bio-oil through multistep extraction into three parts: light oil (26.13%), mid-weight oil (54.19%), and heavy oil (19.68%). These fractions were characterized by gas chromatography-mass spectrometry, Fourier transform infrared spectroscopy, 1H nuclear magnetic resonance spectroscopy, and thermogravimetric analysis. The results showed that most of the highly valued chemicals were contained in the light oil; the mid-weight oil consisted of aromatic oligomer derived from the decomposition of lignin, which could be a promising candidate for partial substitute for petroleumasphalt binder; the heavy oil was rich in alkanes. [ABSTRACT FROM AUTHOR]

Background: Proline-rich tyrosine kinase 2 (Pyk2) is essential in neutrophil degranulation and chemotaxis in vitro. However, its effect on the process of lung inflammation and edema formation during LPS induced acute lung injury (ALI) remains unknown. The goal of the present study was to determine the effect of inhibiting Pyk2 on LPSinduced acute lung inflammation and injury in vivo. Methods: C57BL6 mice were given either 10 mg/kg LPS or saline intratracheally. Inhibition of Pyk2 was effected by intraperitoneal administration TAT-Pyk2-CT 1 h before challenge. Bronchoalveolar lavage analysis of cell counts, lung histology and protein concentration in BAL were analyzed at 18 h after LPS treatment. KC and MIP-2 concentrations in BAL were measured by a mouse cytokine multiplex kit. The static lung compliance was determined by pressure-volume curve using a computer-controlled small animal ventilator. The extravasated Evans blue concentration in lung homogenate was determined spectrophotometrically. Results: Intratracheal instillation of LPS induced significant neutrophil infiltration into the lung interstitium and alveolar space, which was attenuated by pre-treatment with TAT-Pyk2-CT. TAT-Pyk2-CT pretreatment also attenuated 1) myeloperoxidase content in lung tissues, 2) vascular leakage as measured by Evans blue dye extravasation in the lungs and the increase in protein concentration in bronchoalveolar lavage, and 3) the decrease in lung compliance. In each paradigm, treatment with control protein TAT-GFP had no blocking effect. By contrast, production of neutrophil chemokines MIP-2 and keratinocyte-derived chemokine in the bronchoalveolar lavage was not reduced by TAT-Pyk2-CT. Western blot analysis confirmed that tyrosine phosphorylation of Pyk2 in LPSchallenged lungs was reduced to control levels by TAT-Pyk2-CT pretreatment. Conclusions: These results suggest that Pyk2 plays an important role in the development of acute lung injury in mice and that pharmacological inhibition of Pyk2 might provide a potential therapeutic strategy in the pretreatment for patients at imminent risk of developing acute lung injury. [ABSTRACT FROM AUTHOR]

Background: Cytosolic gIVaPLA2 is a critical enzyme in the generation of arachidonate metabolites and in induction of β2-integrin adhesion in granulocytes. We hypothesized that gIVaPLA2 activation also is an essential downstream step for post adhesive migration of PMN in vitro. Methods: Migration of PMNs caused by IL-8/CXCL8 was assessed using a transwell migration chamber. PMNs were pretreated with two structurally unrelated inhibitors of gIVaPLA2, arachidonyl trifluoromethylketone (TFMK) or pyrrophenone, prior to IL-8/CXCL8 exposure. The fraction of migrated PMNs present in the lower chamber was measured as total myeloperoxidase content. GIVaPLA2 enzyme activity was analyzed using [14C-PAPC] as specific substrate F-actin polymerization and cell structure were examined after rhodamine-phalloidin staining. Results: IL-8/CXCL8-induced migration of PMNs was elicited in concentration- and time-dependent manner. Time-related phosphorylation and translocation of cytosolic gIVaPLA2 to the nucleus was observed for PMNs stimulated with IL-8/CXCL8 in concentration sufficient to cause upstream phosphorylation of MAPKs (ERK-½ and p38) and Akt/PKB. Inhibition of gIVaPLA2 corresponded to the magnitude of blockade of PMN migration. Neither AA nor LTB4 secretion was elicited following IL-8/CXCL8 activation. In unstimulated PMNs, F-actin was located diffusely in the cytosol; however, a clear polarized morphology with F-actin-rich ruffles around the edges of the cell was observed after activation with IL-8/CXCL8. Inhibition of gIVaPLA2 blocked change in cell shape and migration caused by IL-8/CXCL8 but did not cause F-actin polymerization or translocation of cytosolic F-actin to inner leaflet of the PMN membrane. Conclusion: We demonstrate that IL-8/CXCL8 causes a) phosphorylation and translocation of cytosolic gIVaPLA2 to the nucleus, b) change in cell shape, c) polymerization of F-actin, and d) chemoattractant/migration of PMN in vitro. Inhibition of gIVaPLA2 blocks the deformability and subsequent migration of PMNs caused by IL-8/CXCL8. Our data suggest that activation of gIVaPLA2 is an essential step in PMN migration in vitro. [ABSTRACT FROM AUTHOR]

An injectable calcium phosphate cement (CPC) with porous structure and excellent anti-washout ability was developed in the study. Citric acid and sodium bicarbonate were added into the CPC powder consisting of tetracalcium phosphate (TTCP) and dicalcium phosphate dihydrate (DCPD) to form macro-pores, then different concentrations of sodium hyaluronate (NaHA) solution, as liquid phase, was added into the cement to investigate its effect on CPC’s performance. The prepared CPCs were tested on workability (injectable time and setting time), mechanical strength, as well as anti-washout ability. The experimental results showed that addition of NaHA not only enhanced the anti-washout ability of the CPC dramatically but also improve its other properties. When NaHA concentration was 0.6 wt%, the injectable time elongated to 15.7 ± 0.6 min, the initial and final setting times were respectively shorten to 18.3 ± 1.2 and 58.7 ± 2.1 min, and the compressive strength were increased to 18.78 ± 1.83 MPa. On the other hand, Addition of NaHA showed little effect on porous structure of the CPC and enhanced its bioactivity obviously, which was confirmed by the apatite formation on its surface after immersion in simulated body fluid (SBF). In conclusion, as an in situ shaped injectable biomaterials, the CPC with appropriate addition of NaHA would notably improve its performance and might be used in minimal invasive surgery for bone repair or reconstruction. [ABSTRACT FROM AUTHOR]

We examined the role of class IA phosphoinositide 3-kinase (PI3K) in the regulation of activation of NADPH oxidase in PMNs and the mechanism of PMN-dependent lung inflammation and microvessel injury induced by the pro-inflammatory cytokine TNF-α. TNF-α stimulation of PMNs resulted in superoxide production that was dependent on CD11b/CD18-mediated PMN adhesion. Additionally, TNF-α induced the association of CD11b/CD18 with the NADPH oxidase subunit Nox2 (gp91phox) and phosphorylation of p47phox, indicating the CD11b/CD18 dependence of NADPH oxidase activation. Transduction of wild-type PMNs with Δp85 protein, a dominant-negative form of the class IA PI3K regulatory subunit, p85α, fused to HIV-TAT (TAT-Δp85) prevented (i) CD11b/CD18-dependent PMN adhesion, (ii) interaction of CD11b/CD18 with Nox2 and phosphorylation of p47phox, and (iii) PMN oxidant production. Furthermore, studies in mice showed that i.v. infusion of TAT-Δp85 significantly reduced the recruitment of PMNs in lungs and increase in lung microvascular permeability induced by TNF-α. We conclude that class IA PI3K serves as a nodal point regulating CD11b/CD18-integrin-dependent PMN adhesion and activation of NADPH oxidase, and leads to oxidant production at sites of PMN adhesion, and the resultant lung microvascular injury in mice. [ABSTRACT FROM AUTHOR]

We wanted to determine whether oxygen radicals open the mitochondrial ATP-dependent potassium channels (K[sub ATP] ) during an ischemic period to reduce cell death and oxidant stress. Chick embryonic cardiomyocytes were used. Cell viability was quantified with propidium iodide (5 μM), and free radicals was measured using 2′,7′-dichlorofluorescin diacetate. Preconditioning was produced by 10 min of simulated ischemia followed by 10 min of reoxygenation. Acetylcholine (1 mM), infused for 10 min instead of preconditioning, reduced cell death similarly (24 ± 5%, n = 7 and 18 ± 2%, n = 7, respectively, vs. controls, 49 ± 6%, n = 8). In control series, 60 min of simulated ischemia and 3 h of reoxygenation generated free radicals more than 300% above the baseline (ischemia: 3.63 ± 0.58, reoxygenation: 3.66 ± 0.47, n = 8). Preconditioning and acetylcholine markedly attenuated the oxidant stress during simulated ischemia (1.18 ± 0.41, n = 6 and 1.34 ± 0.60, n = 7 vs. controls 3.63 ± 0.58, n = 8) and re-oxygenation (1.23 ± 0.36, n = 6 and 1.50 ± 0.59, n = 7 vs. controls 3.66 ± 0.47, n = 8). The protection of acetylcholine was abolished with pretreatment with the antioxidant thiol reductant 2-mercaptopropionyl glycine and posttreatment with 5-hydroxydecanoate, a selective mitochondrial K[sub ATP] channel antagonist (37 ± 7%, n = 7). These results demonstrate that oxygen radicals open mitochondrial K[sub ATP] channels, which mediates the acetylcholine-induced preconditioning effect, and that stimulation of this signaling pathway attenuates oxidant stress.Copyright © 2002 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Examines the regulatory role of cytosolic phospholipase A[sub 2] and phosphatidylinositol-specific phospholipase C in the degranulation of human eosinophils and leukotriene C[sub 4] (LTC[sub 4]) synthesis. Reagents used in the study; Method used to assess eosinophil viability; Regulatory role of protein kinase C in stimulated eosinophil peroxidase release and LTC[sub 4] secretion.

Acidic CO2 electrolysis, enhanced by the introduction of alkali cations, presents a strategic approach for improving carbon efficiency compared to processes conducted in neutral and alkaline environments. However, a significant challenge arises from the dissolution of both organic acids and alkali cations in a strongly acidic feed stream, resulting in a considerable energy penalty for downstream separation. In this study, we investigate the feasibility of using flow-electrode capacitive deionization (FCDI) technology to separate organic acids and recover alkali cations from a strongly acidic feed stream (pH ~ 1). We show that organic acids, such as formic acid and acetic acid, are retained in molecular form in the separation chamber, achieving a rejection rate of over 90% under all conditions. Alkali cations, such as K+ and Cs+, migrate to the cathode chamber in ionic form, with their removal and recovery significantly influenced by their concentration and the pH of the feed stream, but responding differently to the types and concentrations of organic acids. The energy consumption for the removal and recovery of K+ is 4 to 8 times higher than for Cs+, and the charge efficiency is significantly influenced by the types of organic acid products and alkali cations. We conduct a series of electrochemical measurements and analyze the impedance spectroscopy, identifying that hindered mass transfer governed the electrode process. Our findings underscore the potential of FCDI as an advanced downstream separation technology for acidic electrocatalysis processes. [ABSTRACT FROM AUTHOR]

The article offers information on the antitumor response induced by certain inorganic nanoparticles, including needle-shaped hydroxyapatite (n-nHA), granule-shaped hydroxyapatite, and silicon dioxide. These nanoparticles effectively impair tumor progression by triggering the formation of multinucleated giant cells (MNGCs) and promoting macrophage fusion, leading to extensive depletion of tumor-associated macrophages in the tumor microenvironment, thus suppressing tumor growth and metastasis.

The Forkhead box f1 (Foxf1) transcription factor is expressed in mesenchymal cells of the lung, liver, and gallbladder. Although Foxf1 deficiency causes severe abnormalities in the development of these organs, the molecular mechanisms underlying Foxf1 function remain uncharacterized. In this study we inactivated Foxf1 function in lung mesenchymal cells and mouse embryonic fibroblasts (MEFs) by use of either short interfering RNA duplexes or a membrane-transducing Foxf1 dominant negative (DN) mutant protein (Foxf1 DN), the latter of which is fused to the human immunodeficiency virus TAT protein transduction domain. Although Foxf1 did not influence DNA replication or cell survival, Foxf1 depletion severely diminished mesenchyme migration. Foxf1 deficiency in mesenchymal cells was associated with reduced expression of the integrin-beta3 (Itgβ3) subunit. Furthermore, we generated transgenic mice containing a tetracycline-inducible Foxf1 DN transgene. Adenovirus-mediated activation of Foxf1 DN in transgenic MEFs caused diminished cell migration and reduced Itgβ3 expression. A chromatin immunoprecipitation assay demonstrated that Foxf1 protein binds to the bp -871 to -815 region of the mouse Itgβ3 promoter. Deletion of the -871 to -815 Itgβ3 promoter region completely abolished the ability of Foxf1 to activate transcription of the Itgβ3 promoter in cotransfection experiments, indicating that the mouse Itgβ3 is a direct transcriptional target of Foxf1 protein. Foxf1 plays an essential role in mesenchyme migration by transcriptionally regulating Itgβ3. [ABSTRACT FROM AUTHOR]

Nanofluids due to their good thermal conductivity and stability, have been proposed as a way to surpass the performance of currently available heat transfer fluids in the near future. In this work, we focuses on the preparation of nanofluids with excellent stability and thermal conductivity, which a new type of stable bismuth iodate oxide (BiOIO3) (one type of infrared non-linear optical crystal) nanofluids is successfully prepared by using the two-step method. After the initial physical characterization of BiOIO3 particles, five different dispersants are used to disperse the BiOIO3 nanoparticles, and the best performing nanofluids with a zeta potential value of 144.45 and an average particle size of 22.90 nm could be prepared with PVP dispersant. Furthermore, the addition of PVP dispersant in UV-visible experiments smooth the light absorption curve of the nanofluids, reach a peak of 1.1 at around 350 nm. In the most important thermal conductivity test, the value of thermal conductivity of BiOIO3 nanofluid becomes larger with increasing concentration at 50 °C, reaching a maximum value of 1.52 at 0.134 vol.%, which increases by 0.72 over the same volume concentration of TiO2, indicating the importance of the laminar structure. In view of the excellent properties, new laminar structured nanofluids with light-absorbing properties are expected to receive more attention and exploration in the future. [ABSTRACT FROM AUTHOR]

Investigates the importance of nitric oxide and protein kinase in acetylcholine induced cardioprotection. Quantification of cell variability; Attenuation of oxidant stress during ischemia and reoxygenation; Components of acetylcholine generated oxygen radicals.

Preventing pathogenic viral and bacterial transmission in the human environment is critical, especially in potential outbreaks that may be caused by the release of ancient bacteria currently trapped in the permafrost. Existing commercial disinfectants present issues such as a high carbon footprint. This study proposes a sustainable alternative, a bioliquid derived from biomass prepared by hydrothermal liquefaction. Results indicate a high inactivation rate of pathogenic virus and bacteria by the as-prepared bioliquid, such as up to 99.99% for H1N1, H5N1, H7N9 influenza A virus, and Bacillus subtilis var. niger spores and 99.49% for Bacillus anthracis. Inactivation of Escherichia coli and Staphylococcus epidermidis confirmed that low-molecular-weight and low-polarity compounds in bioliquid are potential antibacterial components. High temperatures promoted the production of antibacterial substances via depolymerization and dehydration reactions. Moreover, bioliquid was innoxious as confirmed by the rabbit skin test, and the cost per kilogram of the bioliquid was $0.04427, which is notably lower than that of commercial disinfectants. This study demonstrates the potential of biomass to support our biosafety with greater environmental sustainability. [ABSTRACT FROM AUTHOR]

The article presents a study which created a biomimetic polyetherketoneketone scaffold with functionalized strontium-doped nanohydroxyapatite coating for osteoporotic bone defect applications. Based on the findings, the scaffold has hierarchically porous architecture and mechanical strength similar to those of osteoporotic trabecular bone. The scaffold is a promising development in the treatment of osteoporotic fractures, particularly in older populations.

Lysocardiolipin acyltransferase (LYCAT), a cardiolipin (CL)- remodeling enzyme, is crucial for maintaining normal mitochondrial function and vascular development. Despite the well-characterized role for LYCAT in the regulation of mitochondrial dynamics, its involvement in lung cancer, if any, remains incompletely understood. In this study, in silico analysis of TCGA lung cancer data sets revealed a significant increase in LYCAT expression, which was later corroborated in human lung cancer tissues and immortalized lung cancer cell lines via indirect immunofluorescence and immunoblotting, respectively. Stable knockdown of LYCAT in NSCLC cell lines not only reduced CL and increased monolyso-CL levels but also reduced in vivo tumor growth, as determined by xenograft studies in athymic nude mice. Furthermore, blocking LYCAT activity using a LYCAT mimetic peptide attenuated cell migration, suggesting a novel role for LYCAT activity in promoting NSCLC. Mechanistically, the pro-proliferative effects of LYCAT were mediated by an increase in mitochondrial fusion and a G1/S cell cycle transition, both of which are linked to increased cell proliferation. Taken together, these results demonstrate a novel role for LYCAT in promoting NSCLC and suggest that targeting LYCAT expression or activity in NSCLC may provide new avenues for the therapeutic treatment of lung cancer. [ABSTRACT FROM AUTHOR]

Porcine deltacoronavirus (PDCoV) is a pathogen belonging to the genus Deltacoronavirus that in 2014 caused outbreaks of piglet diarrhea in the United States. To identify suitable therapeutic targets, a more comprehensive understanding of the viral entry pathway is required, particularly of the role of proteases. Here, we identified the proteases that activate the viral spike (S) glycoprotein to initiate cell entry and also pinpointed the host-cellular pathways that PDCoV uses for entry. Our results revealed that cathepsin L (CTSL) and cathepsin B (CTSB) in lysosomes and extracellular trypsin in cell cultures independently activate the S protein for membrane fusion. Pretreating the cells with the lysosomal acidification inhibitor bafilomycin-A1 (Baf-A1) completely inhibited PDCoV entry, and siRNA-mediated ablation of CTSL or CTSB expression significantly reduced viral infection, indicating that PDCoV uses an endosomal pathway for entry. Of note, trypsin treatment of cell cultures also activated PDCoV entry, even when the endosomal pathway was inhibited. This observation indicated that trypsin-induced S protein cleavage and activation in cell cultures enables viral entry directly from the cell surface. Our results provide critical insights into the PDCoV infection mechanism, uncovering two distinct viral entry pathways: one through cathepsin L and cathepsin B in the endosome and another via a protease at the cell surface. Because PDCoV infection sites represent a proteases-rich environment, these findings suggest that endosome inhibitor treatment alone is insufficient to block PDCoV entry into intestinal epithelial cells in vivo. Therefore, approaches that inhibit viral entry from the cell membrane should also be considered. [ABSTRACT FROM AUTHOR]

We previously reported that exogenously added human group V phospholipase A[sub 2] (hVPLA[sub 2]) could elicit leukotriene B[sub 4] biosynthesis in human neutrophils through the activation of group IVA phospholipase A[sub 2] (cPLA[sub 2]) (Kim, Y. J., Kim, K. P., Han, S. K., Munoz, N. M., Zhu, X., Sano, H., Leff, A. R., and Cho, W. (2002) J. Biol. Chem. 277, 36479-36488). In this study, we determined the functional significance and mechanism of the exogenous hVPLA[sub 2]-induced arachidonic acid (AA) release and leukotriene C[sub 4] (LTC[sub 4]) synthesis in isolated human peripheral blood eosinophils. As low a concentration as 10 nM exogenous hVPLA[sub 2] was able to elicit the significant release of AA and LTC[sub 4] from unstimulated eosinophils, which depended on its ability to act on phosphatidylcholine membranes, hVPLA[sub 2] also augmented the release of AA and LTC[sub 4] from eosinophils activated with formyl-Met-Leu-Phe + cytochalasin B. A cellular fluorescent PLA[sub 2] assay showed that hVPLA[sub 2] had a lipolytic action first on the outer plasma membrane and then on the perinuclear region, hVPLA[sub 2] also caused the translocation of 5-lipoxygenase from the cytosol to the nuclear membrane and a 2-fold increase in 5-1ipoxygenase activity. However, hVPLA[sub 2] induced neither the increase in intracellular calcium concentration nor cPLA[sub 2] phosphorylation; consequently, cPLA[sub 2] activity was not affected by hVPLA[sub 2]. Pharmacological inhibition of cPLA[sub 2] and the hVPLA[sub 2]-induced activation of eosinophils derived from the cPLA[sub 2]-deficient mouse corroborated that hVPLA[sub 2] mediates the release of AA and leukotriene in a cPLA[sub 2]-independent manner. As such, this study represents a unique example in which a secretory phospholipase induces the eicosanoid formation in inflammatory cells, completely independent of cPLA[sub 2] activation. [ABSTRACT FROM AUTHOR]

Objective: To investigate the therapeutic effect of Sishen Wan (, SSW) on ulcerative colitis (UC) induced by dinitrobenzene sulfonic acid and its effect on toll-like receptor 2/interleukin-1 receptor-associated kinase-4/nuclear factor-κB (TLR2/IRAK4/NF-κB) sig-naling pathway in colonic tissue., Methods: In this study, 120 Sprague-Dawley rats were randomly divided into blank and model groups. The experimental UC model in rats was established by subcutaneous injection of hydrocortisone + senna gavage for 21 d + dinitrobenzene sulfonic acid (DNBS)/ ethanol solution enema. The successful model rats were randomly divided into the model group; mesalazine (0.36 g/kg) group; and high-, medium-, and low- dose SSW (24, 12, and 6 g/kg) groups. The model and blank groups were gavaged with equal volumes of distilled water once a day for 21 d. The general condition of the rats was observed, and the body mass, fecal properties, and occult blood were recorded for calculating the disease activity index (DAI) score. The colonic tissue of the rats was collected, and its general morphology and pathological form were noted for obtaining the colonic mucosal injury index (CMDI) score. Hematoxylin-eosin staining was used to view the pathological changes of the colon tissue in each group, apoptosis of the cells was detected using terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining, and quantitative real-time polymerase chain reaction was used to measure the expressions of TLR2, myeloid differentiation primary response gene 88 (MyD88), IRAK4, and NF-κB p65 mRNA in the colon tissue. The expressions of TLR2, MyD88, IRAK4, and NF-κB p65 protein were detected using western blotting and immunohistochemistry assay, and the levels of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in the colon tissue were determined using enzyme linked immunosorbent assay., Results: Compared with the blank group, the general condition of the model group was relatively poor. The DAI and CMDI scores of the model group increased significantly (< 0.01), the glands and intestinal mucosa disappeared partially, and several inflammatory cells infiltrated and gathered in the mucosal layer and base layer of the rats in the model group. Furthermore, the cell apoptosis and expression levels of TLR2, MyD88, IRAK4, and NF-κB p65 mRNA and protein in the colon tissue of rats in the model group increased significantly (< 0.01). The levels of IL-1β and TNF-α increased significantly in the colon tissue of rats in the model group (< 0.01). After treatment with SSW, compared with the model group, the general condition of the UC rats improved. Moreover, the DAI and CMDI scores of the UC rats decreased significantly (< 0.05), and the pathological changes in the colon tissue of the UC rats tended to be normal. The cell apoptosis and expression levels of TLR2, MyD88, IRAK4, and NF-κB p65 mRNA and protein in the colon tissue of the UC rats decreased gradually ( < 0.01), and the levels of IL-1β and TNF-α decreased significantly (< 0.01)., Conclusion: SSW can improve the general condition and alleviate the intestinal mucosal injury of UC model rats. Additionally, SSW can inhibit the TLR2/IRAK4/ NF-κB signaling pathway, but further studies are required to confirm it.