Anti-IL-6 Antibody (A29687)

BACKGROUND:

Heat shock protein 27 (HSP 27) is known as a mediator in immune response and has been recently found to be expressed in prostate cancer. This study aimed to investigate the role of HSP27 in inflammatory BPH.

MATERIAL AND METHODS:

Hospitalized BPH patients who received TURP were divided into 4 groups by the presence and degrees of chronic inflammation: non-inflammatory BPH (NI BPH), mild-inflammatory BPH (MI BPH), moderate-inflammatory BPH (MOI BPH), and severe-inflammatory BPH (SI BPH). Expressions of HSP 27, TNF-α, IL-6, and CD3 in prostate tissues and serum of patients were detected by immunohistochemistry and ELISA.

RESULTS:

Expression of HSP27 in BPH with histological inflammation was significantly higher than in non-inflammatory BPH. In inflammatory BPH groups, HSP27 expression gradually increased along with increasing inflammation. There was a significant correlation between the expression of TNF-α, IL-6, CD3 and HSP27 among different inflammatory BPH groups.

CONCLUSIONS:

HSP27 expression level is associated with the degree of chronic inflammation in BPH and may participate in the pathological process in inflammatory BPH.

BACKGROUND:

Although major concerns exist regarding the potential consequences of human exposures to nanoscale carbon black (CB) particles, limited human toxicological data is currently available. The purpose of this study was to evaluate if nanoscale CB particles could be responsible, at least partially, for the altered lung function and inflammation observed in CB workers exposed to nanoscale CB particles.

METHODS:

Scanning Electron Microscopy (SEM), Transmission Electron Microscopy (TEM), and Brunauer-Emmett-Teller were used to characterize CB. Eighty-one CB-exposed male workers and 104 non-exposed male workers were recruited. The pulmonary function test was performed and pro-inflammatory cytokines were evaluated. To further assess the deposition and pulmonary damage induced by CB nanoparticles, male BALB/c mice were exposed to CB for 6 hours per day for 7 or 14 days. The deposition of CB and the pathological changes of the lung tissue in mice were evaluated by paraffin sections and TEM. The cytokines levels in serum and lung tissue of mice were evaluated by ELISA and immunohistochemical staining (IHC).

RESULTS:

SEM and TEM images showed that the CB particles were 30 to 50 nm in size. In the CB workplace, the concentration of CB was 14.90 mg/m³. Among these CB particles, 50.77% were less than 0.523 micrometer, and 99.55% were less than 2.5 micrometer in aerodynamic diameter. The reduction of lung function parameters including FEV1%, FEV/FVC, MMF%, and PEF% in CB workers was observed, and the IL-1β, IL-6, IL-8, MIP-1beta, and TNF- alpha had 2.86-, 6.85-, 1.49-, 3.35-, and 4.87-folds increase in serum of CB workers, respectively. In mice exposed to the aerosol CB, particles were deposited in the lung. The alveolar wall thickened and a large amount of inflammatory cells were observed in lung tissues after CB exposure. IL-6 and IL-8 levels were increased in both serum and lung homogenate.

CONCLUSIONS:

The data strongly suggests that nanoscale CB particles could be responsible for the lung function reduction and pro-inflammatory cytokines secretion in CB workers. These results, therefore, provide the first evidence of a link between human exposure to CB and long-term pulmonary effects.

This work aims to evaluate the anti-neuroinflammatory effects of natural sesquiterpene dimer caruifolin D from Artemisia absinthium L., which is an edible vegetable or traditional medicinal food in East Asia due to its sedation, anti-asthma and antipruritic effects. In this study, we reported that caruifolin D significantly inhibited the productions of various neuroinflammatory mediators from microglia in response to bacterial lipopolysaccharide stimulation. Moreover, anti-inflammatory mechanism study showed that caruifolin D markedly suppressed the production of intracellular reactive oxygen species, which was an important player involved in neuroinflammation, leading to inhibitory effects on the activations of protein kinase C (PKC) and c-Jun N-terminal kinase (JNK), which were two major neuroinflammatory signaling pathways in the brains. Furthermore, caruifolin D protected neurons against microglia-mediated neuronal inflammatory damages by up-regulating neuronal viability and maintaining healthy neuronal morphology. Taken together, these results expanded our knowledge about the anti-neuroinflammatory and neuroprotective mechanism of Artemisia absinthium L., and also suggested that caruifolin D was a major anti-inflammatory component from Artemisia absinthium L., which might be developed as a drug candidate for neuroinflammation-related diseases.

Geniposide (GP), an iridoid glucoside extracted from Gardenia jasminoides Ellis fruits, has been used as a herbal medicine to treat liver and gall bladder disorders for many years. However the mechanism of anti-inflammatory is largely unknown. In this study, GP significantly attenuated inflammation in acute liver injury (ALI) mice model and in lipopolysaccharide (LPS)-induced THP-1 cells. It was demonstrated that GP obviously decreased the expression of Methyl-CpG binding protein 2 (MeCP2) in vivo and in vitro. Knockdown of MeCP2 with siRNA suppressed the expressions of IL-6 and TNF-α, while over-expression of MeCP2 had a proinflammatory effect on the expression of IL-6 and TNF-α in LPS-induced THP-1 cells. Mechanistically, it was indicated that GP had anti-inflammatory effects at least in part, through suppressing MeCP2. Interestingly, GP could attenuate expressions of Sonic hedgehog (Shh) and GLIS family zinc finger 1 (GLIS1) but increase Ptched1 (PTCH1) expression. Similar findings were also demonstrated at the protein level by siRNA MeCP2. Furthermore, over-expression of MeCP2 obviously increased Shh and GLIS1 expressions but reduced PTCH1 expression. Taken together, GP may serve as an effective modulator of MeCP2-hedgehog pathway (Hh)-axis during the pathogenesis of inflammation. Our findings shed light on the potential therapeutic feature of GP in recovering inflammatory diseases.

Astrocytes appear to be important regulators of the inflammatory events that occur in stroke. Sulfiredoxin-1 (Srxn1), an endogenous antioxidant protein, exhibits neuroprotective effects. Although the mechanism by which Srxn1 negatively regulates oxidative and apoptotic pathways has been extensively characterized, the impact of Srxn1 on inflammation has not been well studied. In this study, we used oxygen-glucose deprivation followed by recovery (OGD/R) and hydrogen peroxide (H2O2) to mimic stress from cerebral ischemic damage on primary cultured astrocytes. We found that knockdown of Srxn1 by two shRNAs resulted in decreased cell viability of astrocytes. Decreased level of Srxn1 also correlated with excessive levels of proinflammatory cytokines and chemokines such as TNF-α, MPO, IL-1β, and IL-6. In addition, Srxn1 appeared to influence the strength of TLR4 signaling pathway; the expression of COX-2, IL-6, and NOS2 were strongly induced by OGD/R and H2O2 in astrocyte cultures with Srxn1-shRNAs. Our results suggested that loss of Srxn1 expression in astrocytes may cause excessive activation of inflammatory responses which contribute to OGD/R- and H2O2-induced cell death. Restoring Srxn1 function by gene therapy and/or pharmacology emerges as a promising strategy for the treatment of stroke and other chronic neurodegenerative diseases.

Our previous study demonstrated that Toll-like receptor 4 (TLR4) could act as a co-receptor with annexin A2 (ANX2) mediating anti-β2-glycoprotein I/β2- glycoprotein I (anti-β2GPI/β2GPI) -induced tissue factor (TF) expression in human acute monocytic leukaemia cell line THP-1. In the current study, we further explored the roles of TLR4 and its adaptors, MD-2 and MyD88, as well as nuclear factor kappa B (NF-κB), in anti-β2GPI/β2GPI-induced the activation of THP-1 cells, especially on the expression of some proinflammatory molecules. The results showed that treatment of THP-1 cells with anti-β2GPI (10μg/ml)/β2GPI (100μg/ml) complex could increase IL-6 (interleukin-6), IL-8 (interleukin-8) as well as TNF-α (tumor necrosis factor alpha) expression (both mRNA and protein levels). These effects could be blocked by addition of TAK-242 (5μM), a blocker of signaling transduction mediated by the intracellular domain of TLR4, and also by NF-κB inhibitor PDTC (20μM). Overall, our results indicate that anti-β2GPI/β2GPI complex induced IL-6, IL-8 and TNF-α expression involving TLR4/MD-2/MyD88 and NF-κB signaling pathways and this might be associated with pathological mechanisms of antiphospholipid syndrome (APS).

CONTEXT:

As the first-line agent for genital warts, podophyllotoxin (POD) could induce extensively skin burning, itching, and erythema. Meanwhile, as a common anti-inflammatory agent, glycyrrhizic acid (GA), also has amphipathic and solubilizing properties, indicating that it might be a promising drug carrier.

OBJECTIVE:

The objective of this study is to formulate and characterize the POD-loaded GA micelles preparation and to evaluate its drug release characteristics and anti-inflammatory properties.

MATERIALS AND METHODS:

The novel micelles preparation was prepared by ultrasonic dispersion method and characterized using different scanning calorimetries, dynamic light scattering, and transmission electron microscopies. Subsequently, its encapsulation efficiency (EE), drug-loading content (LC), in vitro skin permeation, in vivo drug retention, and distribution of POD were detected. The anti-inflammatory effect of the preparation was reflected by HE staining and immunohistochemistry in the rat skin.

RESULTS:

The POD-loaded GA micelles formed spherical shapes (approximately 10 nm) with an EE of 78.53 ± 2.17% and a LC of 7.293 ± 0.42%. Meaningfully, unlike the extensive distribution of the POD tincture throughout the skin tissue, POD released from the POD-loaded GA micelles mainly located in the epidermis and could maintain steady skin retention for 12 h. Moreover, the POD-loaded GA micelles induced less leukocyte infiltration and inflammatory factors (IL-6 and TNF-α) expression when compared with the POD tincture.

DISCUSSION AND CONCLUSION:

Our results suggested that the POD-loaded GA micelles could achieve a higher POD distribution in the epidermal layer as well as a lighter skin inflammation. This new POD delivery system might be a potential and promising candidate for genital warts and deserved further researches.